Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury
Identifieur interne : 000441 ( Pmc/Checkpoint ); précédent : 000440; suivant : 000442Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury
Auteurs : Sara J. Holditch ; Carolyn N. Brown ; Andrew M. Lombardi ; Khoa N. Nguyen ; Charles L. EdelsteinSource :
- International Journal of Molecular Sciences [ 1422-0067 ] ; 2019.
Abstract
Cisplatin is a widely used chemotherapeutic agent used to treat solid tumours, such as ovarian, head and neck, and testicular germ cell. A known complication of cisplatin administration is acute kidney injury (AKI). The development of effective tumour interventions with reduced nephrotoxicity relies heavily on understanding the molecular pathophysiology of cisplatin-induced AKI. Rodent models have provided mechanistic insight into the pathophysiology of cisplatin-induced AKI. In the subsequent review, we provide a detailed discussion of recent advances in the cisplatin-induced AKI phenotype, principal mechanistic findings of injury and therapy, and pre-clinical use of AKI rodent models. Cisplatin-induced AKI murine models faithfully develop gross manifestations of clinical AKI such as decreased kidney function, increased expression of tubular injury biomarkers, and tubular injury evident by histology. Pathways involved in AKI include apoptosis, necrosis, inflammation, and increased oxidative stress, ultimately providing a translational platform for testing the therapeutic efficacy of potential interventions. This review provides a discussion of the foundation laid by cisplatin-induced AKI rodent models for our current understanding of AKI molecular pathophysiology.
Url:
DOI: 10.3390/ijms20123011
PubMed: 31226747
PubMed Central: 6627318
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury</title><author><name sortKey="Holditch, Sara J" sort="Holditch, Sara J" uniqKey="Holditch S" first="Sara J." last="Holditch">Sara J. Holditch</name></author><author><name sortKey="Brown, Carolyn N" sort="Brown, Carolyn N" uniqKey="Brown C" first="Carolyn N." last="Brown">Carolyn N. Brown</name></author><author><name sortKey="Lombardi, Andrew M" sort="Lombardi, Andrew M" uniqKey="Lombardi A" first="Andrew M." last="Lombardi">Andrew M. Lombardi</name></author><author><name sortKey="Nguyen, Khoa N" sort="Nguyen, Khoa N" uniqKey="Nguyen K" first="Khoa N." last="Nguyen">Khoa N. Nguyen</name></author><author><name sortKey="Edelstein, Charles L" sort="Edelstein, Charles L" uniqKey="Edelstein C" first="Charles L." last="Edelstein">Charles L. 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Holditch</name></author><author><name sortKey="Brown, Carolyn N" sort="Brown, Carolyn N" uniqKey="Brown C" first="Carolyn N." last="Brown">Carolyn N. Brown</name></author><author><name sortKey="Lombardi, Andrew M" sort="Lombardi, Andrew M" uniqKey="Lombardi A" first="Andrew M." last="Lombardi">Andrew M. Lombardi</name></author><author><name sortKey="Nguyen, Khoa N" sort="Nguyen, Khoa N" uniqKey="Nguyen K" first="Khoa N." last="Nguyen">Khoa N. Nguyen</name></author><author><name sortKey="Edelstein, Charles L" sort="Edelstein, Charles L" uniqKey="Edelstein C" first="Charles L." last="Edelstein">Charles L. Edelstein</name></author></analytic><series><title level="j">International Journal of Molecular Sciences</title><idno type="eISSN">1422-0067</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>Cisplatin is a widely used chemotherapeutic agent used to treat solid tumours, such as ovarian, head and neck, and testicular germ cell. A known complication of cisplatin administration is acute kidney injury (AKI). The development of effective tumour interventions with reduced nephrotoxicity relies heavily on understanding the molecular pathophysiology of cisplatin-induced AKI. Rodent models have provided mechanistic insight into the pathophysiology of cisplatin-induced AKI. In the subsequent review, we provide a detailed discussion of recent advances in the cisplatin-induced AKI phenotype, principal mechanistic findings of injury and therapy, and pre-clinical use of AKI rodent models. Cisplatin-induced AKI murine models faithfully develop gross manifestations of clinical AKI such as decreased kidney function, increased expression of tubular injury biomarkers, and tubular injury evident by histology. Pathways involved in AKI include apoptosis, necrosis, inflammation, and increased oxidative stress, ultimately providing a translational platform for testing the therapeutic efficacy of potential interventions. This review provides a discussion of the foundation laid by cisplatin-induced AKI rodent models for our current understanding of AKI molecular pathophysiology.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Dasari, S" uniqKey="Dasari S">S. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Int J Mol Sci</journal-id><journal-id journal-id-type="iso-abbrev">Int J Mol Sci</journal-id><journal-id journal-id-type="publisher-id">ijms</journal-id><journal-title-group><journal-title>International Journal of Molecular Sciences</journal-title></journal-title-group><issn pub-type="epub">1422-0067</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31226747</article-id><article-id pub-id-type="pmc">6627318</article-id><article-id pub-id-type="doi">10.3390/ijms20123011</article-id><article-id pub-id-type="publisher-id">ijms-20-03011</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Recent Advances in Models, Mechanisms, Biomarkers, and Interventions in Cisplatin-Induced Acute Kidney Injury</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Holditch</surname><given-names>Sara J.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Brown</surname><given-names>Carolyn N.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Lombardi</surname><given-names>Andrew M.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Nguyen</surname><given-names>Khoa N.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Edelstein</surname><given-names>Charles L.</given-names></name><xref rid="c1-ijms-20-03011" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-ijms-20-03011">Division of Renal Diseases and Hypertension, University of Colorado at Denver, Box C281, 12700 East, 19th Ave, Aurora, CO 80045, USA;<email>sara.holditch@ucdenver.edu</email> (S.J.H.);<email>CAROLYN.N.BROWN@UCDENVER.EDU</email> (C.N.B.);<email>anlo5057@colorado.edu</email> (A.M.L.);<email>KHOA.N.NGUYEN@UCDENVER.EDU</email> (K.N.N.)</aff><author-notes><corresp id="c1-ijms-20-03011"><label>*</label>Correspondence: <email>Charles.edelstein@ucdenver.edu</email>; Tel.: +303-724-4810; Fax: +303-724-4868</corresp></author-notes><pub-date pub-type="epub"><day>20</day><month>6</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>6</month><year>2019</year></pub-date><volume>20</volume><issue>12</issue><elocation-id>3011</elocation-id><history><date date-type="received"><day>10</day><month>5</month><year>2019</year></date><date date-type="accepted"><day>12</day><month>6</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Cisplatin is a widely used chemotherapeutic agent used to treat solid tumours, such as ovarian, head and neck, and testicular germ cell. A known complication of cisplatin administration is acute kidney injury (AKI). The development of effective tumour interventions with reduced nephrotoxicity relies heavily on understanding the molecular pathophysiology of cisplatin-induced AKI. Rodent models have provided mechanistic insight into the pathophysiology of cisplatin-induced AKI. In the subsequent review, we provide a detailed discussion of recent advances in the cisplatin-induced AKI phenotype, principal mechanistic findings of injury and therapy, and pre-clinical use of AKI rodent models. Cisplatin-induced AKI murine models faithfully develop gross manifestations of clinical AKI such as decreased kidney function, increased expression of tubular injury biomarkers, and tubular injury evident by histology. Pathways involved in AKI include apoptosis, necrosis, inflammation, and increased oxidative stress, ultimately providing a translational platform for testing the therapeutic efficacy of potential interventions. This review provides a discussion of the foundation laid by cisplatin-induced AKI rodent models for our current understanding of AKI molecular pathophysiology.</p></abstract><kwd-group><kwd>cisplatin</kwd><kwd>acute kidney injury</kwd><kwd>AKI</kwd><kwd>apoptosis</kwd><kwd>inflammation</kwd><kwd>oxidative stress</kwd></kwd-group></article-meta></front><floats-group><fig id="ijms-20-03011-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>The complex pathophysiology of cisplatin-induced AKI. (I.) autophagosome/lysosome. (II.) mitochondria (III.) fragmented DNA (cell death). Abbreviations: organic cation transporters (OCTs), multidrug resistance-associated proteins (MRPs), multi-antimicrobial extrusion protein (MATEs), chemokine (C-X-C motif) ligand (CXCL), chemokine (C-C motif) ligand (CCL), interleukin-1 beta (IL-1β), tumour necrosis factor (TNF). blood urea nitrogen (BUN), serum creatinine (SCr) kidney injury molecule-1 (KIM-1), neutrophil gelatinase –associated lipocalin (NGAL), interleukin-18 (IL-18).</p></caption><graphic xlink:href="ijms-20-03011-g001"></graphic></fig><table-wrap id="ijms-20-03011-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">ijms-20-03011-t001_Table 1</object-id><label>Table 1</label><caption><p>Routine and novel biomarkers of cisplatin-induced AKI.</p></caption><table frame="hsides" rules="groups"><thead><tr><th rowspan="2" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin;border-left:solid thin;border-right:solid thin" colspan="1">Type</th><th colspan="6" align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin;border-right:solid thin;background:#E7E6E6" rowspan="1">Model</th></tr><tr><th colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1">Low Dose, Short-Term</th><th colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1">Low Dose, Long-Term</th><th colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1">High Dose, Short-Term</th></tr></thead><tbody><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Cisplatin dosage</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1">5–15 mg/kg</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1">5–15 mg/kg</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1">20–30 mg/kg</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Study duration</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1"><7 Days</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1">>7 Days</td><td colspan="2" align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1"><7 Days</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Routine AKI biomarker</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">BUN [<xref rid="B33-ijms-20-03011" ref-type="bibr">33</xref>] (40–60 mg/dL)<break></break>SCr [<xref rid="B34-ijms-20-03011" ref-type="bibr">34</xref>] (0.1–0.5 mg/dL)</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">** Cystatin-C [<xref rid="B35-ijms-20-03011" ref-type="bibr">35</xref>] (1–1.3 µg/mL)<break></break>KIM-1 [<xref rid="B36-ijms-20-03011" ref-type="bibr">36</xref>] (10–12 fold increase)<break></break>NGAL [<xref rid="B37-ijms-20-03011" ref-type="bibr">37</xref>] (0.3–1.3 µg/mL)<break></break>CCL2 [<xref rid="B38-ijms-20-03011" ref-type="bibr">38</xref>] (0.5–10 fold increase mRNA)</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">BUN [<xref rid="B39-ijms-20-03011" ref-type="bibr">39</xref>] (30–150 mg/dL)<break></break>SCr [<xref rid="B40-ijms-20-03011" ref-type="bibr">40</xref>] (0.5–3 mg/dL)</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">KIM-1 [<xref rid="B41-ijms-20-03011" ref-type="bibr">41</xref>] (0.05–0.1 mg/mL)<break></break>NGAL [<xref rid="B41-ijms-20-03011" ref-type="bibr">41</xref>] (20–40 mg/mL)</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">BUN [<xref rid="B42-ijms-20-03011" ref-type="bibr">42</xref>] (50–200 mg/dL)<break></break>SCr [<xref rid="B43-ijms-20-03011" ref-type="bibr">43</xref>] (0.5–3 mg/dL)</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">* Cystatin-C [<xref rid="B44-ijms-20-03011" ref-type="bibr">44</xref>] (14–18 ng/mL)<break></break>KIM-1 [<xref rid="B45-ijms-20-03011" ref-type="bibr">45</xref>] 50–100 fold increased)<break></break>NGAL/SCr [<xref rid="B46-ijms-20-03011" ref-type="bibr">46</xref>] (6–10 µg/mg)<break></break>CCL2 [<xref rid="B46-ijms-20-03011" ref-type="bibr">46</xref>] (10–30 fold increase mRNA)<break></break>IL-18 [<xref rid="B47-ijms-20-03011" ref-type="bibr">47</xref>] (20–25 pg/mg)</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Timing of detection</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">>48 h</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>72 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">>48 h</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>72 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">>48 h</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>72 h</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Novel AKI biomarker</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">miRNAs [<xref rid="B5-ijms-20-03011" ref-type="bibr">5</xref>] (10 fold increase): miR-130a, 151–3p, 218, 320, 680, 138, 152, 221, 328, 685</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Urinary Wnt4 [<xref rid="B48-ijms-20-03011" ref-type="bibr">48</xref>] (0.1–0.7 µg/mg)<break></break>Urinary ARL13B [<xref rid="B49-ijms-20-03011" ref-type="bibr">49</xref>] (15–45 fold increase)</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">N/A</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Renal IL-33 [<xref rid="B50-ijms-20-03011" ref-type="bibr">50</xref>] (0.3–1.0 µg/mg)</td><td align="center" valign="middle" style="border-bottom:solid thin;background:#F2F2F2" rowspan="1" colspan="1">N/A</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Urinary NGAL [<xref rid="B51-ijms-20-03011" ref-type="bibr">51</xref>] (40–120 units/g SCr)<break></break>Urinary FasL [<xref rid="B52-ijms-20-03011" ref-type="bibr">52</xref>] (45–150 pg/mL)<break></break>Renal IL-33 [<xref rid="B50-ijms-20-03011" ref-type="bibr">50</xref>] (0.3–1.0 µg/mg)</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin;border-left:solid thin;border-right:solid thin;background:#F2F2F2" rowspan="1" colspan="1">Timing of detection</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"><24 h</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>24 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">N/A</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>24 h</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">N/A</td><td align="center" valign="middle" style="border-bottom:solid thin;border-right:solid thin" rowspan="1" colspan="1">>24 h</td></tr></tbody></table><table-wrap-foot><fn><p>Hours, hrs. Blood Urea Nitrogen, BUN. Kidney Injury Molecule-1, KIM1. Neutrophil Gelatinase-Associated Lipocalin, NGAL. Chemokine ligand 2, CCL2. Fas Ligand, FasL. Interleukin 33, IL-33. N-acetyl-β-d-glucosaminidase, NAG. Interleukin 18, IL-18. Creatinine, SCr. ADP Ribosylation Factor Like GTPase 13B, ARL13B. MicroRNA, MiRNA. * Mouse, ** Rat.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc><affiliations><list></list><tree><noCountry><name sortKey="Brown, Carolyn N" sort="Brown, Carolyn N" uniqKey="Brown C" first="Carolyn N." last="Brown">Carolyn N. Brown</name><name sortKey="Edelstein, Charles L" sort="Edelstein, Charles L" uniqKey="Edelstein C" first="Charles L." last="Edelstein">Charles L. Edelstein</name><name sortKey="Holditch, Sara J" sort="Holditch, Sara J" uniqKey="Holditch S" first="Sara J." last="Holditch">Sara J. Holditch</name><name sortKey="Lombardi, Andrew M" sort="Lombardi, Andrew M" uniqKey="Lombardi A" first="Andrew M." last="Lombardi">Andrew M. Lombardi</name><name sortKey="Nguyen, Khoa N" sort="Nguyen, Khoa N" uniqKey="Nguyen K" first="Khoa N." last="Nguyen">Khoa N. Nguyen</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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