Serveur d'exploration Chloroquine

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Autophagy in Immune-Related Renal Disease

Identifieur interne : 000971 ( Pmc/Checkpoint ); précédent : 000970; suivant : 000972

Autophagy in Immune-Related Renal Disease

Auteurs : Xin Ye [République populaire de Chine] ; Xu-Jie Zhou [République populaire de Chine] ; Hong Zhang [République populaire de Chine]

Source :

RBID : PMC:6878805

Abstract

Autophagy is an important biology process, central to the maintenance of biology process in both physiological and pathological situations. It is regarded as a “double-edged sword”—exerting both protective and/or detrimental effects. These two-way effects are observed in immune cells as well as renal resident cells, including podocytes, mesangial cells, tubular epithelial cells, and endothelial cells of the glomerular capillaries. Mounting evidence suggests that autophagy is implicated in the pathological process of various immune-related renal diseases (IRRDs) as well as the kidney that underwent transplantation. Here, we provide an overview of the pathological role of autophagy in IRRDs, including lupus nephritis, IgA nephropathy, membrane nephropathy, ANCA-associated nephritis, and diabetic nephropathy. The understanding of the pathogenesis and regulatory mechanisms of autophagy in these renal diseases may lead to the identification of new diagnostic targets and refined therapeutic modulation.


Url:
DOI: 10.1155/2019/5071687
PubMed: 31815154
PubMed Central: 6878805


Affiliations:


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PMC:6878805

Le document en format XML

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</TEI>
<pmc article-type="review-article">
<pmc-dir>properties open_access</pmc-dir>
<front>
<journal-meta>
<journal-id journal-id-type="nlm-ta">J Immunol Res</journal-id>
<journal-id journal-id-type="iso-abbrev">J Immunol Res</journal-id>
<journal-id journal-id-type="publisher-id">JIR</journal-id>
<journal-title-group>
<journal-title>Journal of Immunology Research</journal-title>
</journal-title-group>
<issn pub-type="ppub">2314-8861</issn>
<issn pub-type="epub">2314-7156</issn>
<publisher>
<publisher-name>Hindawi</publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id pub-id-type="pmid">31815154</article-id>
<article-id pub-id-type="pmc">6878805</article-id>
<article-id pub-id-type="doi">10.1155/2019/5071687</article-id>
<article-categories>
<subj-group subj-group-type="heading">
<subject>Review Article</subject>
</subj-group>
</article-categories>
<title-group>
<article-title>Autophagy in Immune-Related Renal Disease</article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname>Ye</surname>
<given-names>Xin</given-names>
</name>
<xref ref-type="aff" rid="I1"></xref>
</contrib>
<contrib contrib-type="author" corresp="yes">
<contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0002-7215-707X</contrib-id>
<name>
<surname>Zhou</surname>
<given-names>Xu-jie</given-names>
</name>
<email>zhouxujie@bjmu.edu.cn</email>
<xref ref-type="aff" rid="I1"></xref>
</contrib>
<contrib contrib-type="author">
<contrib-id contrib-id-type="orcid" authenticated="false">https://orcid.org/0000-0001-9855-4068</contrib-id>
<name>
<surname>Zhang</surname>
<given-names>Hong</given-names>
</name>
<xref ref-type="aff" rid="I1"></xref>
</contrib>
</contrib-group>
<aff id="I1">Renal Division, Peking University First Hospital, Peking University Institute of Nephrology, Key Laboratory of Renal Disease, Ministry of Health of China, Key Laboratory of Chronic Kidney Disease Prevention and Treatment (Peking University), Ministry of Education, Beijing 100034, China</aff>
<author-notes>
<fn fn-type="other">
<p>Guest Editor: Minggang Zhang</p>
</fn>
</author-notes>
<pub-date pub-type="collection">
<year>2019</year>
</pub-date>
<pub-date pub-type="epub">
<day>7</day>
<month>11</month>
<year>2019</year>
</pub-date>
<volume>2019</volume>
<elocation-id>5071687</elocation-id>
<history>
<date date-type="received">
<day>25</day>
<month>8</month>
<year>2019</year>
</date>
<date date-type="accepted">
<day>8</day>
<month>10</month>
<year>2019</year>
</date>
</history>
<permissions>
<copyright-statement>Copyright © 2019 Xin Ye 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>Autophagy is an important biology process, central to the maintenance of biology process in both physiological and pathological situations. It is regarded as a “double-edged sword”—exerting both protective and/or detrimental effects. These two-way effects are observed in immune cells as well as renal resident cells, including podocytes, mesangial cells, tubular epithelial cells, and endothelial cells of the glomerular capillaries. Mounting evidence suggests that autophagy is implicated in the pathological process of various immune-related renal diseases (IRRDs) as well as the kidney that underwent transplantation. Here, we provide an overview of the pathological role of autophagy in IRRDs, including lupus nephritis, IgA nephropathy, membrane nephropathy, ANCA-associated nephritis, and diabetic nephropathy. The understanding of the pathogenesis and regulatory mechanisms of autophagy in these renal diseases may lead to the identification of new diagnostic targets and refined therapeutic modulation.</p>
</abstract>
<funding-group>
<award-group>
<funding-source>University of Michigan Health System–Peking University Health Science Center Joint Institute for Translational and Clinical Research</funding-source>
<award-id>BMU2017JI007</award-id>
</award-group>
<award-group>
<funding-source>Natural Science Foundation for Innovation Research Group of China</funding-source>
<award-id>81621092</award-id>
</award-group>
<award-group>
<funding-source>National Key Research and Development Program of China</funding-source>
<award-id>2016YFC0904102</award-id>
</award-group>
<award-group>
<funding-source>National Natural Science Foundation of China</funding-source>
<award-id>91642120</award-id>
<award-id>81570629</award-id>
</award-group>
<award-group>
<funding-source>Beijing Youth Top-notch Talent Support Program</funding-source>
<award-id>2017000021223ZK31</award-id>
</award-group>
<award-group>
<funding-source>Beijing Nova Program</funding-source>
<award-id>Z171100001117023</award-id>
</award-group>
<award-group>
<funding-source>Beijing Municipal Natural Science Foundation</funding-source>
<award-id>Z190023</award-id>
</award-group>
</funding-group>
</article-meta>
</front>
<floats-group>
<fig id="fig1" orientation="portrait" position="float">
<label>Figure 1</label>
<caption>
<p>Immune-related renal disease. Aberrant immunity, such as autoimmune diseases, is a systemic disease. These immune disruptions, such as autoantibody production, immune complex formation, and disposition, can cause damage to any organ of our body, such as the heart, the lung, and the joints. However, the kidneys are susceptible to these immune-mediated damages, which results from its unique hemodynamic characteristics, kidney-specific DAMPs, and crystal formation in the tubule system. Besides, the renal resident cells, including podocytes, glomerular capillary epithelial cells, tubule epithelial cells, and mesangial, are also found to be susceptible to immune-mediated injuries.</p>
</caption>
<graphic xlink:href="JIR2019-5071687.001"></graphic>
</fig>
<fig id="fig2" orientation="portrait" position="float">
<label>Figure 2</label>
<caption>
<p>Classic autophagy pathway. There are three major types of classic autophagy process in mammalians: macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Macroautophagy includes four major steps: induction, elongation, and maturation of autophagosome and fusion with lysosome. Several protein complexes are involved in this process.</p>
</caption>
<graphic xlink:href="JIR2019-5071687.002"></graphic>
</fig>
<fig id="fig3" orientation="portrait" position="float">
<label>Figure 3</label>
<caption>
<p>Autophagy in renal resident cells. The figure summarizes current studies of autophagy in renal resident cells, including podocytes, glomerular capillary epithelial cells, mesangial cells, and tubule epithelial cells. Upregulation or downregulation of autophagy activity through gene expression modulation or under certain stimulation can influence the survival of these cells and the overall function of the kidney. Taken together, autophagy plays a protective role in the physiology and pathophysiology of the kidney.</p>
</caption>
<graphic xlink:href="JIR2019-5071687.003"></graphic>
</fig>
<fig id="fig4" orientation="portrait" position="float">
<label>Figure 4</label>
<caption>
<p>Autophagy dysfunction in lupus nephritis. Macrophagy eliminates neutrophil extracellular trap (NET) through autophagy. Autophagy deficiency in macrophagy leads to DNA exposure of NET, which activates adaptive immunity and produces anti-dsDNA antibodies. Autophagy dysfunction in podocytes fails to clear the autoantibodies, which subsequently binds to DNA fractions of NETs, forming immune complexes. These immune complexes will damage kidney and cause nephritis in lupus.</p>
</caption>
<graphic xlink:href="JIR2019-5071687.004"></graphic>
</fig>
<table-wrap id="tab1" orientation="portrait" position="float">
<label>Table 1</label>
<caption>
<p>Autophagy's role in immune cells and renal resident cells.</p>
</caption>
<table frame="hsides" rules="groups">
<thead>
<tr>
<th rowspan="1" colspan="1"></th>
<th align="center" rowspan="1" colspan="1">Cell type</th>
<th align="center" rowspan="1" colspan="1">Role of autophagy</th>
<th align="center" rowspan="1" colspan="1">Ref.</th>
</tr>
</thead>
<tbody>
<tr>
<td align="left" rowspan="4" colspan="1">Immune cells</td>
<td align="center" rowspan="1" colspan="1">Macrophage</td>
<td align="center" rowspan="1" colspan="1">Helps control inflammation and contributes to caspase-independent cell death</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B6" ref-type="bibr">6</xref>
,
<xref rid="B7" ref-type="bibr">7</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">Dendritic cell</td>
<td align="center" rowspan="1" colspan="1">Required for virus detection, antigen presentation, and inferon production</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B8" ref-type="bibr">8</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">T cell</td>
<td align="center" rowspan="1" colspan="1">Promotes survival and cytokine secretion</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B11" ref-type="bibr">11</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">B cell</td>
<td align="center" rowspan="1" colspan="1">Contributes to B cell differentiation and cell death</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B12" ref-type="bibr">12</xref>
,
<xref rid="B13" ref-type="bibr">13</xref>
]</td>
</tr>
<tr>
<td align="center" colspan="4" rowspan="1">
<hr></hr>
</td>
</tr>
<tr>
<td align="left" rowspan="4" colspan="1">Renal resident cells</td>
<td align="center" rowspan="1" colspan="1">Podocyte</td>
<td align="center" rowspan="1" colspan="1">Autophagy dysfunction is associated with clinical proteinuria and decreased renal function</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B17" ref-type="bibr">17</xref>
,
<xref rid="B24" ref-type="bibr">24</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">Capillary endothelial cell</td>
<td align="center" rowspan="1" colspan="1">Protects endothelial from ROS</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B26" ref-type="bibr">26</xref>
,
<xref rid="B27" ref-type="bibr">27</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">Mesangial cell</td>
<td align="center" rowspan="1" colspan="1">Protects mesangial cell from ROS and contributes to cell survival</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B30" ref-type="bibr">30</xref>
,
<xref rid="B31" ref-type="bibr">31</xref>
]</td>
</tr>
<tr>
<td align="center" rowspan="1" colspan="1">TEC</td>
<td align="center" rowspan="1" colspan="1">Promotes TEC survival and helps eliminate toxins; contributes to renal fibrosis and nephropathic cystinosis</td>
<td align="center" rowspan="1" colspan="1">[
<xref rid="B32" ref-type="bibr">32</xref>
,
<xref rid="B40" ref-type="bibr">40</xref>
]</td>
</tr>
</tbody>
</table>
</table-wrap>
</floats-group>
</pmc>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
<settlement>
<li>Pékin</li>
</settlement>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Ye, Xin" sort="Ye, Xin" uniqKey="Ye X" first="Xin" last="Ye">Xin Ye</name>
</noRegion>
<name sortKey="Zhang, Hong" sort="Zhang, Hong" uniqKey="Zhang H" first="Hong" last="Zhang">Hong Zhang</name>
<name sortKey="Zhou, Xu Jie" sort="Zhou, Xu Jie" uniqKey="Zhou X" first="Xu-Jie" last="Zhou">Xu-Jie Zhou</name>
</country>
</tree>
</affiliations>
</record>

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