Roles of Inflammasomes in Inflammatory Kidney Diseases
Identifieur interne : 000406 ( Pmc/Checkpoint ); précédent : 000405; suivant : 000407Roles of Inflammasomes in Inflammatory Kidney Diseases
Auteurs : Jinjin Fan [République populaire de Chine] ; Kaifeng Xie [République populaire de Chine] ; Liqin Wang [République populaire de Chine] ; Nuoyan Zheng [République populaire de Chine] ; Xueqing Yu [République populaire de Chine]Source :
- Mediators of Inflammation [ 0962-9351 ] ; 2019.
Abstract
The immune system has a central role in eliminating detrimental factors, by frequently launching inflammatory responses towards pathogen infection and inner danger signal outbreak. Acute and chronic inflammatory responses are critical determinants for consequences of kidney diseases, in which inflammasomes were inevitably involved. Inflammasomes are closely linked to many kidney diseases such as acute kidney injury and chronic kidney diseases. Inflammasomes are macromolecules consisting of multiple proteins, and their formation initiates the cleavage of procaspase-1, resulting in the activation of gasdermin D as well as the maturation and release of interleukin-1
Url:
DOI: 10.1155/2019/2923072
PubMed: 31427885
PubMed Central: 6679869
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Roles of Inflammasomes in Inflammatory Kidney Diseases</title><author><name sortKey="Fan, Jinjin" sort="Fan, Jinjin" uniqKey="Fan J" first="Jinjin" last="Fan">Jinjin Fan</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Xie, Kaifeng" sort="Xie, Kaifeng" uniqKey="Xie K" first="Kaifeng" last="Xie">Kaifeng Xie</name><affiliation wicri:level="1"><nlm:aff id="I2">Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Guangdong Medical University, Zhanjiang, Guangdong Province 524001</wicri:regionArea><wicri:noRegion>Guangdong Province 524001</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Liqin" sort="Wang, Liqin" uniqKey="Wang L" first="Liqin" last="Wang">Liqin Wang</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Nuoyan" sort="Zheng, Nuoyan" uniqKey="Zheng N" first="Nuoyan" last="Zheng">Nuoyan Zheng</name><affiliation wicri:level="1"><nlm:aff id="I4">Translational Medical Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Translational Medical Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Xueqing" sort="Yu, Xueqing" uniqKey="Yu X" first="Xueqing" last="Yu">Xueqing Yu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31427885</idno><idno type="pmc">6679869</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6679869</idno><idno type="RBID">PMC:6679869</idno><idno type="doi">10.1155/2019/2923072</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000A62</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000A62</idno><idno type="wicri:Area/Pmc/Curation">000A62</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000A62</idno><idno type="wicri:Area/Pmc/Checkpoint">000406</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000406</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Roles of Inflammasomes in Inflammatory Kidney Diseases</title><author><name sortKey="Fan, Jinjin" sort="Fan, Jinjin" uniqKey="Fan J" first="Jinjin" last="Fan">Jinjin Fan</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Xie, Kaifeng" sort="Xie, Kaifeng" uniqKey="Xie K" first="Kaifeng" last="Xie">Kaifeng Xie</name><affiliation wicri:level="1"><nlm:aff id="I2">Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Guangdong Medical University, Zhanjiang, Guangdong Province 524001</wicri:regionArea><wicri:noRegion>Guangdong Province 524001</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Liqin" sort="Wang, Liqin" uniqKey="Wang L" first="Liqin" last="Wang">Liqin Wang</name><affiliation wicri:level="1"><nlm:aff id="I3">Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Zheng, Nuoyan" sort="Zheng, Nuoyan" uniqKey="Zheng N" first="Nuoyan" last="Zheng">Nuoyan Zheng</name><affiliation wicri:level="1"><nlm:aff id="I4">Translational Medical Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Translational Medical Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author><author><name sortKey="Yu, Xueqing" sort="Yu, Xueqing" uniqKey="Yu X" first="Xueqing" last="Yu">Xueqing Yu</name><affiliation wicri:level="1"><nlm:aff id="I1">Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</nlm:aff><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000</wicri:regionArea><wicri:noRegion>Guangdong Province 510000</wicri:noRegion></affiliation></author></analytic><series><title level="j">Mediators of Inflammation</title><idno type="ISSN">0962-9351</idno><idno type="eISSN">1466-1861</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The immune system has a central role in eliminating detrimental factors, by frequently launching inflammatory responses towards pathogen infection and inner danger signal outbreak. Acute and chronic inflammatory responses are critical determinants for consequences of kidney diseases, in which inflammasomes were inevitably involved. Inflammasomes are closely linked to many kidney diseases such as acute kidney injury and chronic kidney diseases. Inflammasomes are macromolecules consisting of multiple proteins, and their formation initiates the cleavage of procaspase-1, resulting in the activation of gasdermin D as well as the maturation and release of interleukin-1<italic>β</italic> and IL-18, leading to pyroptosis. Here, we discuss the mechanism in which inflammasomes occur, as well as their roles in inflammatory kidney diseases, in order to shed light for discovering new therapeutical targets for the prevention and treatment of inflammatory kidney diseases and consequent end-stage renal disease.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Martinon, F" uniqKey="Martinon F">F. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Mediators Inflamm</journal-id><journal-id journal-id-type="iso-abbrev">Mediators Inflamm</journal-id><journal-id journal-id-type="publisher-id">MI</journal-id><journal-title-group><journal-title>Mediators of Inflammation</journal-title></journal-title-group><issn pub-type="ppub">0962-9351</issn><issn pub-type="epub">1466-1861</issn><publisher><publisher-name>Hindawi</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31427885</article-id><article-id pub-id-type="pmc">6679869</article-id><article-id pub-id-type="doi">10.1155/2019/2923072</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review Article</subject></subj-group></article-categories><title-group><article-title>Roles of Inflammasomes in Inflammatory Kidney Diseases</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Fan</surname><given-names>Jinjin</given-names></name><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib><contrib contrib-type="author"><name><surname>Xie</surname><given-names>Kaifeng</given-names></name><xref ref-type="aff" rid="I2"><sup>2</sup></xref></contrib><contrib contrib-type="author"><name><surname>Wang</surname><given-names>Liqin</given-names></name><xref ref-type="aff" rid="I3"><sup>3</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-6032-8815</contrib-id><name><surname>Zheng</surname><given-names>Nuoyan</given-names></name><email>zhnuoy@mail.sysu.edu.cn</email><xref ref-type="aff" rid="I4"><sup>4</sup></xref></contrib><contrib contrib-type="author" corresp="yes"><contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-8624-744X</contrib-id><name><surname>Yu</surname><given-names>Xueqing</given-names></name><email>yuxq@mail.sysu.edu.cn</email><xref ref-type="aff" rid="I1"><sup>1</sup></xref></contrib></contrib-group><aff id="I1"><sup>1</sup>Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</aff><aff id="I2"><sup>2</sup>Guangdong Medical University, Zhanjiang, Guangdong Province 524001, China</aff><aff id="I3"><sup>3</sup>Department of Radiology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</aff><aff id="I4"><sup>4</sup>Translational Medical Center, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510000, China</aff><author-notes><fn fn-type="other"><p>Academic Editor: Robson Coutinho-Silva</p></fn></author-notes><pub-date pub-type="collection"><year>2019</year></pub-date><pub-date pub-type="epub"><day>21</day><month>7</month><year>2019</year></pub-date><volume>2019</volume><elocation-id>2923072</elocation-id><history><date date-type="received"><day>20</day><month>3</month><year>2019</year></date><date date-type="accepted"><day>11</day><month>6</month><year>2019</year></date></history><permissions><copyright-statement>Copyright © 2019 Jinjin Fan et al.</copyright-statement><copyright-year>2019</copyright-year><license xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p></license></permissions><abstract><p>The immune system has a central role in eliminating detrimental factors, by frequently launching inflammatory responses towards pathogen infection and inner danger signal outbreak. Acute and chronic inflammatory responses are critical determinants for consequences of kidney diseases, in which inflammasomes were inevitably involved. Inflammasomes are closely linked to many kidney diseases such as acute kidney injury and chronic kidney diseases. Inflammasomes are macromolecules consisting of multiple proteins, and their formation initiates the cleavage of procaspase-1, resulting in the activation of gasdermin D as well as the maturation and release of interleukin-1<italic>β</italic> and IL-18, leading to pyroptosis. Here, we discuss the mechanism in which inflammasomes occur, as well as their roles in inflammatory kidney diseases, in order to shed light for discovering new therapeutical targets for the prevention and treatment of inflammatory kidney diseases and consequent end-stage renal disease.</p></abstract><funding-group><award-group><funding-source>Science and Technology Planning Project of Guangdong Province of China</funding-source><award-id>A2018042</award-id></award-group><award-group><funding-source>National Natural Science Foundation of China</funding-source><award-id>31200664</award-id></award-group><award-group><funding-source>National Key R&D Program of China</funding-source><award-id>2016YFC0906101</award-id></award-group></funding-group></article-meta></front><floats-group><fig id="fig1" orientation="portrait" position="float"><label>Figure 1</label><caption><p>Schematic illustration of the role of inflammasomes in lupus nephritis. ATP released from dead cells activates P2X7 on the cell membrane, inducing the K<sup>+</sup> efflux and NLRP3 inflammasome assembly. The assembly of NLRP3 inflammasomes and maturation of caspase-1 caused the cleavage of pro-IL-18 and pro-IL-1<italic>β</italic>, as well as the release of the N-terminal gasdermin D to induce pyroptosis. The neutrophil extracellular trap releases a large amount of dsDNA and other cellular components and induces the formation of a dsDNA-containing immune complex, which promotes the activation of NLRP3 inflammasomes via TLRs. The endogenous RNA-containing complex can also activate NLRP3 inflammasomes through the endosome-located TLR7/8 signaling pathway. AIM2 and another IFI family member IFI16 can sense/recognize dsDNA, leading to the activation of caspase-1 and maturation of IL-18 and IL-1<italic>β</italic>. The signature cytokine of lupus, IFN-<italic>α</italic>, binds to IFN receptors on the cell surface, which regulate the expression and maximum activity of AIM2 inflammasomes. Released IL-1<italic>β</italic>, IL-18, and other inflammatory mediators resulted in endothelial leakage, immune cell infiltration, and finally tissue inflammation and functional deterioration of the kidney.</p></caption><graphic xlink:href="MI2019-2923072.001"></graphic></fig><table-wrap id="tab1" orientation="portrait" position="float"><label>Table 1</label><caption><p>Roles of inflammasomes in inflammatory kidney diseases.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Disease</th><th align="center" rowspan="1" colspan="1">Inflammasomes involved</th><th align="center" rowspan="1" colspan="1">Roles and potential mechanism</th><th align="center" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="left" rowspan="3" colspan="1">Acute kidney injury</td><td align="center" rowspan="3" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1"><italic>Nlrp3</italic> gene deletion protected mice from AKI.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B143" ref-type="bibr">143</xref>, <xref rid="B144" ref-type="bibr">144</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">ATP-sensitive P2X7 receptor activates the NLRP3 inflammasomes.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B145" ref-type="bibr">145</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Cell debris (histones, HGBM1, etc.) mediated NLRP3 inflammasome activation.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B70" ref-type="bibr">70</xref>, <xref rid="B72" ref-type="bibr">72</xref>, <xref rid="B74" ref-type="bibr">74</xref>]</td></tr><tr><td align="center" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="4" colspan="1">IgA nephropathy</td><td align="center" rowspan="4" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1"><italic>Nlrp3</italic> deficiency improved renal function and renal injury in a mouse IgAN model.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B85" ref-type="bibr">85</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1"><italic>NLRP3</italic> gene expression was correlated with clinical outcome in IgAN patients.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B82" ref-type="bibr">82</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">IgA-immune complexes activated NLRP3 inflammasomes involving ROS production in macrophages, dendritic cells, and renal intrinsic cells.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B85" ref-type="bibr">85</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Generation of ROS and activation of NF-<italic>κ</italic>B lead to NLRP3 activation, which is a key event in IgAN.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B84" ref-type="bibr">84</xref>]</td></tr><tr><td align="center" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="6" colspan="1">Diabetic nephropathy</td><td align="center" rowspan="5" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1"><italic>Nlrp3</italic>-deficient mice are protected against diabetic nephropathy.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B88" ref-type="bibr">88</xref>, <xref rid="B89" ref-type="bibr">89</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Mitochondrial ROS, TLR4 signaling, and NLRP3 inflammasome activation aggravate diabetic nephropathy.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B89" ref-type="bibr">89</xref>, <xref rid="B91" ref-type="bibr">91</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">TXNIP activated NLRP3 inflammasomes in podocytes of diabetic nephropathy.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B95" ref-type="bibr">95</xref>, <xref rid="B146" ref-type="bibr">146</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">High glucose and LPS activate ROS/TXNIP/NLRP3/IL-1<italic>β</italic> inflammasome signaling in glomerular mesangial cells.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B96" ref-type="bibr">96</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">ATP-P2X4 signaling mediated high glucose-induced activation of NLRP3 inflammasomes.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B90" ref-type="bibr">90</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">NLRC4</td><td align="center" rowspan="1" colspan="1"><italic>Nlrc4</italic> deficiency resulted in diminished disease progression in diabetic mice. Activation of NF-<italic>κ</italic>B and MAPK pathways was blocked by <italic>Nlrc4</italic> deficiency.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B98" ref-type="bibr">98</xref>]</td></tr><tr><td align="center" colspan="4" rowspan="1"><hr></hr></td></tr><tr><td align="left" rowspan="7" colspan="1">Lupus nephritis</td><td align="center" rowspan="1" colspan="1">NLRP1</td><td align="center" rowspan="1" colspan="1">Polymorphism of <italic>NLRP1</italic> was related to the pathogenesis of lupus.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B119" ref-type="bibr">119</xref>]</td></tr><tr><td align="center" rowspan="3" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">NLRP3 inflammasomes were activated in podocytes from NZM2328 mice and patients of LN; P2X7/NLRP3 is a key signaling pathway.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B110" ref-type="bibr">110</xref>, <xref rid="B111" ref-type="bibr">111</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Immune complex containing dsDNA induced IL-1<italic>β</italic> production through NLRP3 inflammasomes.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B104" ref-type="bibr">104</xref>, <xref rid="B105" ref-type="bibr">105</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Lack of NLRP3 enhanced lupus symptom in B6<sup>lpr</sup> mice by inhibiting TGF target genes.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B114" ref-type="bibr">114</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">AIM2</td><td align="center" rowspan="1" colspan="1"><italic>AIM2</italic> expression was increased in lupus patients and closely correlated with the severity of disease in SLE patients. AIM2 facilitates the apoptotic DNA-induced lupus damage via arbitrating macrophage functional maturation.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B100" ref-type="bibr">100</xref>, <xref rid="B131" ref-type="bibr">131</xref>]</td></tr><tr><td align="center" rowspan="2" colspan="1">IFI16</td><td align="center" rowspan="1" colspan="1">IFI16 expression was increased in leukocytes but not in kidney biopsies of lupus patients.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B129" ref-type="bibr">129</xref>, <xref rid="B131" ref-type="bibr">131</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Anti-IFI16 antibody titers were higher in lupus patients and inversely correlated with proteinuria.</td><td align="center" rowspan="1" colspan="1">[<xref rid="B110" ref-type="bibr">110</xref>]</td></tr></tbody></table></table-wrap><table-wrap id="tab2" orientation="portrait" position="float"><label>Table 2</label><caption><p>Expression profiles of inflammasome members in PBMCs of IgAN patients.</p></caption><table frame="hsides" rules="groups"><thead><tr><th rowspan="1" colspan="1"></th><th align="center" rowspan="1" colspan="1">Healthy donors<break></break><italic>n</italic> = 17</th><th align="center" rowspan="1" colspan="1">IgAN patients<break></break><italic>n</italic> = 22</th><th align="center" rowspan="1" colspan="1"><italic>P</italic> value</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">Gender</td><td align="center" rowspan="1" colspan="1">F8/M9</td><td align="center" rowspan="1" colspan="1">F15/M7</td><td align="center" rowspan="1" colspan="1">0.19</td></tr><tr><td align="left" rowspan="1" colspan="1">Age</td><td align="center" rowspan="1" colspan="1">34.9 ± 9.3</td><td align="center" rowspan="1" colspan="1">32 ± 10.3</td><td align="center" rowspan="1" colspan="1">0.38</td></tr><tr><td align="left" rowspan="1" colspan="1">CREA</td><td align="center" rowspan="1" colspan="1">56.2 ± 10.4</td><td align="center" rowspan="1" colspan="1">87 ± 38.3</td><td align="center" rowspan="1" colspan="1">0.007<sup>∗∗</sup></td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>NLRP1</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.062 ± 0.003</td><td align="center" rowspan="1" colspan="1">0.068 ± 0.005</td><td align="center" rowspan="1" colspan="1">0.42</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>NLRP3</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.018 ± 0.0007</td><td align="center" rowspan="1" colspan="1">0.028 ± 0.003</td><td align="center" rowspan="1" colspan="1">0.014<sup>∗</sup></td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>NLRC4</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.016 ± 0.0010</td><td align="center" rowspan="1" colspan="1">0.015 ± 0.0015</td><td align="center" rowspan="1" colspan="1">0.64</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>NAIP</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.069 ± 0.006</td><td align="center" rowspan="1" colspan="1">0.07 ± 0.005</td><td align="center" rowspan="1" colspan="1">0.69</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>AIM2</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.0035 ± 0.0003</td><td align="center" rowspan="1" colspan="1">0.0032 ± 0.0005</td><td align="center" rowspan="1" colspan="1">0.68</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>PYRIN</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.07 ± 0.005</td><td align="center" rowspan="1" colspan="1">0.08 ± 0.009</td><td align="center" rowspan="1" colspan="1">0.30</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>IFI16</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.13 ± 0.012</td><td align="center" rowspan="1" colspan="1">0.10 ± 0.011</td><td align="center" rowspan="1" colspan="1">0.08</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>ASC</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.18 ± 0.02</td><td align="center" rowspan="1" colspan="1">0.16 ± 0.019</td><td align="center" rowspan="1" colspan="1">0.47</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>Caspase-1</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.17 ± 0.02</td><td align="center" rowspan="1" colspan="1">0.12 ± 0.002</td><td align="center" rowspan="1" colspan="1">0.41</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>IL-1β</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.015 ± 0.0016</td><td align="center" rowspan="1" colspan="1">0.011 ± 0.0012</td><td align="center" rowspan="1" colspan="1">0.10</td></tr><tr><td align="left" rowspan="1" colspan="1"><italic>IL-18</italic> mRNA levels</td><td align="center" rowspan="1" colspan="1">0.012 ± 0.002</td><td align="center" rowspan="1" colspan="1">0.010 ± 0.001</td><td align="center" rowspan="1" colspan="1">0.49</td></tr></tbody></table><table-wrap-foot><fn><p>Verified healthy donors and primary IgAN patients were enrolled under the supervision of the Ethics Review Committee of the First Affiliated Hospital, Sun Yat-sen University (Guangzhou, China), and this study was conducted in accordance with the guidelines proposed in the Declaration of Helsinki. None of the patients had been treated with steroids and/or immunosuppressive drugs within one year nor did they show clinical infection symptoms at the day when blood samples were taken. PBMCs from venous blood with anticoagulant EDTA-K2 were enriched and subjected to RNA extraction. Gene expression was analyzed with real-time PCR analysis and calculated with the 2<sup>-<italic>ΔΔ</italic>Ct</sup> method, using <italic>GAPDH</italic> as the internal control. Sequences and primers for each genes were acquired from the NCBI database (<ext-link ext-link-type="uri" xlink:href="https://www.ncbi.nlm.nih.gov">https://www.ncbi.nlm.nih.gov</ext-link>). All statistical assessments were two-sided using a significance value of <italic>P</italic> < 0.05 (indicated as ∗) and <italic>P</italic> < 0.01 (indicated as ∗∗).</p></fn></table-wrap-foot></table-wrap><table-wrap id="tab3" orientation="portrait" position="float"><label>Table 3</label><caption><p>Compounds targeting inflammasomes for kidney diseases.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="left" rowspan="1" colspan="1">Compound</th><th align="center" rowspan="1" colspan="1">Inflammasome target</th><th align="center" rowspan="1" colspan="1">Disease/animal model</th><th align="center" rowspan="1" colspan="1">Reference</th></tr></thead><tbody><tr><td align="left" rowspan="1" colspan="1">BAY 11-7082 (NF-<italic>κ</italic>B inhibitor)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Paraquat-induced acute kidney injury model (rat)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B147" ref-type="bibr">147</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Allopurinol (oxidase inhibitor)</td><td align="center" rowspan="1" colspan="1">Need to be specified</td><td align="center" rowspan="1" colspan="1">Glycerol-induced acute kidney injury model (rat)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B148" ref-type="bibr">148</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">4-Hydroxycinnamaldehyde-galactosamine</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">LPS-induced renal inflammation (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B149" ref-type="bibr">149</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Harmine</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">LPS-induced renal inflammation model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B150" ref-type="bibr">150</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Artemisinin</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">5/6 nephrectomy (rat)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B151" ref-type="bibr">151</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Rotenone (inhibitor of mitochondrial complex I)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Aldosterone-infused renal nephropathy model (rat)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B152" ref-type="bibr">152</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Hydroxychloroquine</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Ischemia-reperfusion model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B73" ref-type="bibr">73</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">1,3-Butanediol (inhibitor of the NLRP3)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Nephrocalcinosis-related chronic kidney disease model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B153" ref-type="bibr">153</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">CP-456773 (inhibitor of the NLRP3)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Oxalate- or adenine-induced crystal nephropathy</td><td align="center" rowspan="1" colspan="1">[<xref rid="B154" ref-type="bibr">154</xref>]</td></tr><tr><td align="left" rowspan="2" colspan="1">Ginsenoside compound K</td><td align="center" rowspan="2" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">High-fat diet/streptozotocin-induced diabetic nephritis (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B155" ref-type="bibr">155</xref>]</td></tr><tr><td align="center" rowspan="1" colspan="1">Unilateral ureteral obstruction model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B156" ref-type="bibr">156</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">FL-926-16 (carnosine derivative)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">db/db diabetic mice</td><td align="center" rowspan="1" colspan="1">[<xref rid="B157" ref-type="bibr">157</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Verapamil</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Diabetic nephropathy</td><td align="center" rowspan="1" colspan="1">[<xref rid="B158" ref-type="bibr">158</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Osthole</td><td align="center" rowspan="3" colspan="1">NLRP3</td><td align="center" rowspan="3" colspan="1">A progressive IgAN model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B84" ref-type="bibr">84</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Antroquinonol</td><td align="center" rowspan="1" colspan="1">[<xref rid="B83" ref-type="bibr">83</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Resveratrol</td><td align="center" rowspan="1" colspan="1">[<xref rid="B159" ref-type="bibr">159</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Citral</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">LPS-induced accelerated and severe lupus nephritis model (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B112" ref-type="bibr">112</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Piperine</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Pristine-induced lupus nephritis (mice)</td><td align="center" rowspan="1" colspan="1">[<xref rid="B160" ref-type="bibr">160</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Curcumin</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">Lupus-prone female MRL/lpr mice</td><td align="center" rowspan="1" colspan="1">[<xref rid="B161" ref-type="bibr">161</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">Brilliant blue G (P2X7 antagonist)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">NZM2328 lupus-prone mice</td><td align="center" rowspan="1" colspan="1">[<xref rid="B110" ref-type="bibr">110</xref>]</td></tr><tr><td align="left" rowspan="1" colspan="1">MCC950 (inhibitor of NLRP3)</td><td align="center" rowspan="1" colspan="1">NLRP3</td><td align="center" rowspan="1" colspan="1">NZM2328 lupus-prone mice</td><td align="center" rowspan="1" colspan="1">[<xref rid="B111" ref-type="bibr">111</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Fan, Jinjin" sort="Fan, Jinjin" uniqKey="Fan J" first="Jinjin" last="Fan">Jinjin Fan</name></noRegion><name sortKey="Wang, Liqin" sort="Wang, Liqin" uniqKey="Wang L" first="Liqin" last="Wang">Liqin Wang</name><name sortKey="Xie, Kaifeng" sort="Xie, Kaifeng" uniqKey="Xie K" first="Kaifeng" last="Xie">Kaifeng Xie</name><name sortKey="Yu, Xueqing" sort="Yu, Xueqing" uniqKey="Yu X" first="Xueqing" last="Yu">Xueqing Yu</name><name sortKey="Zheng, Nuoyan" sort="Zheng, Nuoyan" uniqKey="Zheng N" first="Nuoyan" last="Zheng">Nuoyan Zheng</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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