The DOI matches its Crossref record; 36 of the 36 references it cites were found in a registry or an index.
Sirtuin 3–dependent mitochondrial dynamic improvements protect against acute kidney injury
Open accessAbstract
Acute kidney injury (AKI) is a public health concern with an annual mortality rate that exceeds those of breast and prostate cancer, heart failure, and diabetes combined. Oxidative stress and mitochondrial damage are drivers of AKI-associated pathology; however, the pathways that mediate these events are poorly defined. Here, using a murine cisplatin-induced AKI model, we determined that both oxidative stress and mitochondrial damage are associated with reduced levels of renal sirtuin 3 (SIRT3). Treatment with the AMPK agonist AICAR or the antioxidant agent acetyl-l-carnitine (ALCAR) restored SIRT3 expression and activity, improved renal function, and decreased tubular injury in WT animals, but had no effect in Sirt3-/- mice. Moreover, Sirt3-deficient mice given cisplatin experienced more severe AKI than WT animals and died, and neither AICAR nor ALCAR treatment prevented death in Sirt3-/- AKI mice. In cultured human tubular cells, cisplatin reduced SIRT3, resulting in mitochondrial fragmentation, while restoration of SIRT3 with AICAR and ALCAR improved cisplatin-induced mitochondrial dysfunction. Together, our results indicate that SIRT3 is protective against AKI and suggest that enhancing SIRT3 to improve mitochondrial dynamics has potential as a strategy for improving outcomes of renal injury.
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Cites
AMPK regulates energy expenditure by modulating NAD+ metabolism and SIRT1 activity
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Cellular pathophysiology of ischemic acute kidney injury
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Stereological Methods. Practical methods for biological morphometry
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Mitochondrial form and function
Friedman, J. R., & Nunnari, J. (2014) · Nature · doi:10.1038/nature12985 · Cited by 1,803 · cited 2×
“Another element tipping the balance toward fusion is the SIRT3-induced upregulation of OPA1, which mediates the fusion of the inner membrane of the organelle (8, 26, 27).”
Practical methods for biological morphometry
Weibel, E. R. (1979) · Academic Press eBooks · Cited by 1,563
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Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation
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Cited by
NAD+ metabolism: pathophysiologic mechanisms and therapeutic potential
Xie, N., Zhang, L., Gao, W., Huang, C., Huber, P. E., Zhou, X., Li, C., Shen, G., & Zou, B. (2020) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-020-00311-7 · Cited by 1,052
Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence
Rajman, L., Chwalek, K., & Sinclair, D. A. (2018) · Cell Metabolism · doi:10.1016/j.cmet.2018.02.011 · Cited by 865
NAD+ homeostasis in health and disease
Katsyuba, E., Romani, M., Hofer, D., & Auwerx, J. (2020) · Nature Metabolism · doi:10.1038/s42255-019-0161-5 · Cited by 627
Cisplatin nephrotoxicity: new insights and therapeutic implications
Tang, C., Livingston, M. J., Safirstein, R., & Dong, Z. (2023) · Nature Reviews Nephrology · doi:10.1038/s41581-022-00631-7 · Cited by 548
Mitochondrial quality control in kidney injury and repair
Tang, C., Cai, J., Yin, X.-M., Weinberg, J. M., Venkatachalam, M. A., & Dong, Z. (2021) · Nature Reviews Nephrology · doi:10.1038/s41581-020-00369-0 · Cited by 513
Metadata
- Authors
- Morigi, M., Perico, L., Rota, C., Longaretti, L., Conti, S., Rottoli, D., Novelli, R., Remuzzi, G., & Benigni, A.
- Venue
- Journal of Clinical Investigation
- Published
- 2015-01-20
- Volume
- 125
- Issue
- 2
- Pages
- 715-726
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W1969475086
- Cited by
- 403
- References
- 36
- FWCI
- 27.69
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Morigi, M., Perico, L., Rota, C., Longaretti, L., Conti, S., Rottoli, D., Novelli, R., Remuzzi, G., & Benigni, A. (2015). Sirtuin 3–dependent mitochondrial dynamic improvements protect against acute kidney injury. Journal of Clinical Investigation. https://doi.org/10.1172/jci77632
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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