The DOI matches its Crossref record; 58 of the 58 references it cites were found in a registry or an index.
Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models
Open accessAbstract
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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“For example, mitochondrial fission occurs in the kidneys and heart after acute ischemia/reperfusion injury in mice, and prevention of this process is beneficial (5, 32).”
From Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2012) · cites this paper as [5]
In the citing paper
“For example, mitochondrial fission occurs in the kidneys and heart after acute ischemia/reperfusion injury in mice, and prevention of this process is beneficial (5, 32).”
From Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2012) · cites this paper as [5]
In the citing paper
“Moreover, these studies revealed that silencing of Drp1 expression was not associated with reduced translocation of the pro-apoptotic protein Bax to mitochondria, suggesting that Drp1 functions downstream of Bax during apoptosis.”
From New insights into the role of mitochondria in aging: mitochondrial dynamics and more (2010) · cites this paper as Brooks et al., 2009
In the citing paper
“The role of mitochondrial dynamics in regulating apoptosis is mainly based on the finding that overexpression of the dominant-negative mutant Drp1K38A induces mitochondrial fusion and confers resistance to apoptosis by preventing a loss of Δψm and inhibiting cytochrome c release (Breckenridge et al., 2003; Brooks et al., 2009; Frank et al., 2001; Karbowski et al., 2002).”
From New insights into the role of mitochondria in aging: mitochondrial dynamics and more (2010) · cites this paper as Brooks et al., 2009
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Citations
Cites
The BCL-2 protein family: opposing activities that mediate cell death
Youle, R. J., & Strasser, A. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2308 · Cited by 4,806
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(2001) · PubMed · Cited by 2,381
Cisplatin nephrotoxicity: Mechanisms and renoprotective strategies
Pabla, N., & Dong, Z. (2008) · Kidney International · doi:10.1038/sj.ki.5002786 · Cited by 1,959
Self-citationDynamin-related Protein Drp1 Is Required for Mitochondrial Division in Mammalian Cells
Smirnova, E., Griparić, L., Shurland, D., & van der Bliek, A. M. (2001) · Molecular Biology of the Cell · doi:10.1091/mbc.12.8.2245 · Cited by 1,938
Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction
Chen, H., Chomyn, A., & Chan, D. C. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m503062200 · Cited by 1,376
Mitochondrial dynamics and apoptosis
Suen, D.-F., Norris, K. L., & Youle, R. J. (2008) · Genes & Development · doi:10.1101/gad.1658508 · Cited by 1,270
Cassidy-Stone, A., Chipuk, J. E., Ingerman, E., Song, C., Yoo, C., Kuwana, T., Kurth, M. J., Shaw, J. T., Hinshaw, J. E., Green, D. R., et al. (2008) · Developmental Cell · doi:10.1016/j.devcel.2007.11.019 · Cited by 1,200
Cribbs, J. T., & Strack, S. (2007) · EMBO Reports · doi:10.1038/sj.embor.7401062 · Cited by 1,061
Roles of the mammalian mitochondrial fission and fusion mediators Fis1, Drp1, and Opa1 in apoptosis
Lee, Y.-J., Jeong, S.-Y., Karbowski, M., Smith, C. L., & Youle, R. J. (2004) · Molecular Biology of the Cell · doi:10.1091/mbc.e04-04-0294 · Cited by 1,042
Research works printed but not linked: 1
- Wang, 2001, Genes Dev., 15, 2922
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Mitochondria: In Sickness and in Health
Nunnari, J., & Suomalainen, A. (2012) · Cell · doi:10.1016/j.cell.2012.02.035 · Cited by 3,479
“…and drug toxicities are also associatedwith increasedmitochondrial fragmentation in cultured cells models and in animal models of myocardial infarction and drug induced renal toxicity, inhibition of mitochondrial division has shown therapeutic promise (Brooks et al., 2009; Ong et al., 2010).”
BackgroundMechanisms of Diabetic Complications
Forbes, J. M., & Cooper, M. E. (2013) · Physiological Reviews · doi:10.1152/physrev.00045.2011 · Cited by 2,890
“This suggests that although mitochondrial abnormalities may be early manifestations of the disease, the ultimate loss of ATP generation is likely to contribute to end-organ decline and cell death in the later stages of disease progression (64, 578).”
BackgroundThe cell biology of mitochondrial membrane dynamics
Giacomello, M., Pyakurel, A., Glytsou, C., & Scorrano, L. (2020) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-020-0210-7 · Cited by 1,550
Mitochondrial energetics in the kidney
Bhargava, P., & Schnellmann, R. G. (2017) · Nature Reviews Nephrology · doi:10.1038/nrneph.2017.107 · Cited by 1,391
Pathophysiology of Acute Kidney Injury
Basile, D. P., Anderson, M. D., & Sutton, T. A. (2012) · Comprehensive physiology · doi:10.1002/cphy.c110041 · Cited by 1,256
“Mitochondrial fission is more pronounced following ATP depletion in cultured proximal tubule cells and this change is thought to contribute to outer membrane permeabilizataion and consequent apoptosis (76).”
Metadata
- Authors
- Brooks, C., Wei, Q., Cho, S.-G., & Dong, Z.
- Affiliations
- Charlie Norwood VA Medical Center (US)
- Corresponding author
- Dong, Zheng
- Venue
- Journal of Clinical Investigation
- Published
- 2009-05-01
- Volume
- 119
- Issue
- 5
- Pages
- 1275-1285
- ISSN
- 0021-9738 (ISSN-L)
- 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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