Cited by 735Mitochondrial Function and PathologyCell death mechanisms and regulationAutophagy in Disease and Therapy

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Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models

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Brooks, Craig, Wei, Qingqing, Cho, Sung-Gyu, Dong, Zheng·2009·Journal of Clinical Investigation

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Abstract

The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. Here, we have demonstrated a striking morphological change of mitochondria in experimental models of renal ischemia/reperfusion and cisplatin-induced nephrotoxicity. This change contributed to mitochondrial outer membrane permeabilization, release of apoptogenic factors, and consequent apoptosis. Following either ATP depletion or cisplatin treatment of rat renal tubular cells, mitochondrial fragmentation was observed prior to cytochrome c release and apoptosis. This mitochondrial fragmentation was inhibited by Bcl2 but not by caspase inhibitors. Dynamin-related protein 1 (Drp1), a critical mitochondrial fission protein, translocated to mitochondria early during tubular cell injury, and both siRNA knockdown of Drp1 and expression of a dominant-negative Drp1 attenuated mitochondrial fragmentation, cytochrome c release, caspase activation, and apoptosis. Further in vivo analysis revealed that mitochondrial fragmentation also occurred in proximal tubular cells in mice during renal ischemia/reperfusion and cisplatin-induced nephrotoxicity. Notably, both tubular cell apoptosis and acute kidney injury were attenuated by mdivi-1, a newly identified pharmacological inhibitor of Drp1. This study demonstrates a rapid regulation of mitochondrial dynamics during acute kidney injury and identifies mitochondrial fragmentation as what we believe to be a novel mechanism contributing to mitochondrial damage and apoptosis in vivo in mouse models of disease.

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Authors: Brooks, C., Wei, Q., Cho, S.-G., & Dong, Z.
Affiliations: Charlie Norwood VA Medical Center (US)
Corresponding author: Dong, Zheng
ORCID: Brooks, Craig
Wei, Qingqing
Cho, Sung-Gyu
Dong, Zheng
Venue: Journal of Clinical Investigation
Publisher: American Society for Clinical Investigation
Published: 2009-05-01
Volume: 119
Issue: 5
Pages: 1275-1285
ISSN: 0021-9738 (ISSN-L)
DOI: 10.1172/jci37829
PMC: PMC2673870
OpenAlex: W2155978870
Cited by: 735
References: 58
Citations by year: 2026: 24 · 2025: 31 · 2024: 51 · 2023: 34 · 2022: 59 · 2021: 49 · 2020: 64 · 2019: 59 · 2018: 43 · 2017: 54 · 2016: 42 · 2015: 40 · 2014: 45 · 2013: 36 · 2012: 41
FWCI: 13.84
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Journal of Clinical Investigation (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: U.S. Department of Veterans Affairs
Brigham and Women's Hospital
Silence Therapeutics
National Institutes of Health
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
Keywords: mitochondrial dynamics, mitochondrial fragmentation, acute kidney injury, apoptosis, mitochondrial outer membrane permeabilization, cytochrome c release, Drp1, Mdivi-1, renal ischemia-reperfusion, cisplatin nephrotoxicity, Bcl-2, caspase activation, ATP depletion
MeSH terms: Adenosine Triphosphate, Animals, Cell Line, Cells, Cultured, Cisplatin, Enzyme Inhibitors, Kidney Tubular Necrosis, Acute, Kidney Tubules, Proximal, Male, Mice, Inbred C57BL, Microtubule-Associated Proteins, Mitochondria, Reperfusion Injury, Apoptosis, Proto-Oncogene Proteins c-bcl-2, Sodium Azide, GTP Phosphohydrolases, Imaging, Three-Dimensional, Dynamins, RNA, Small Interfering, Cytochromes c, Mice, Rats, Caspase Inhibitors

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Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models

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