ArticleAmerican journal of physiology. Renal physiology2009
Anaphylatoxin C5a contributes to the pathogenesis of cisplatin-induced nephrotoxicity.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 39 citations in OpenAlex.
- Complement in acute kidney injury: a convergent pathogenic pathway in multifactorial renal damage.Frontiers in immunology · 2026Review
- Single-cell RNA sequencing data analysis of the inner ear in gentamicin-treated mice via intraperitoneal injection.Open medicine (Warsaw, Poland) · 2025Article
- Optimizing the cumulative cisplatin dose for concurrent chemoradiotherapy beneficiaries among elderly nasopharyngeal carcinoma patients: a real world study.Scientific reports · 2024Article
- Determination of the optimal concentration and duration of C5aR antagonist application in an inflammatory model of human dental pulp cells.FEBS open bio · 2023Article
- Article
- Kaempferol ameliorates Cisplatin induced nephrotoxicity by modulating oxidative stress, inflammation and apoptosis via ERK and NF-κB pathways.AMB Express · 2020Article
- Isoorientin Attenuates Cisplatin-Induced Nephrotoxicity Through the Inhibition of Oxidative Stress and Apoptosis via Activating the SIRT1/SIRT6/Nrf-2 Pathway.Frontiers in pharmacology · 2020Article
- Time-dependent C5a and C5aR expression in dental pulp cells following stimulation with LTA and LPS.International journal of molecular medicine · 2019Article
- Farrerol Attenuates Cisplatin-Induced Nephrotoxicity by Inhibiting the Reactive Oxygen Species-Mediated Oxidation, Inflammation, and Apoptotic Signaling Pathways.Frontiers in physiology · 2019Article
- Celastrol ameliorates cisplatin nephrotoxicity by inhibiting NF-κB and improving mitochondrial function.EBioMedicine · 2018Article
- Cisplatin-Induced Rodent Model of Kidney Injury: Characteristics and Challenges.BioMed research international · 2018Review
- Ameliorative Effect of Daidzein on Cisplatin-Induced Nephrotoxicity in Mice via Modulation of Inflammation, Oxidative Stress, and Cell Death.Oxidative medicine and cellular longevity · 2017Article
- Cannabidiol Limits T Cell-Mediated Chronic Autoimmune Myocarditis: Implications to Autoimmune Disorders and Organ Transplantation.Molecular medicine (Cambridge, Mass.) · 2016Article
- Article
- Magnesium protects against cisplatin-induced acute kidney injury by regulating platinum accumulation.American journal of physiology. Renal physiology · 2014Article
- Renal interstitial fibrosis: mechanisms and evaluation.Current opinion in nephrology and hypertension · 2012Review
- Pathogenesis of acute kidney injury: foundation for clinical practice.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2011Review
- Renal fibrosis: novel insights into mechanisms and therapeutic targets.Nature reviews. Nephrology · 2010Review
- CB1 cannabinoid receptors promote oxidative/nitrosative stress, inflammation and cell death in a murine nephropathy model.British journal of pharmacology · 2010Article
- Cannabinoid-2 receptor limits inflammation, oxidative/nitrosative stress, and cell death in nephropathy.Free radical biology & medicine · 2010Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Nephrotoxicity is a common complication of cisplatin chemotherapy that limits its clinical use; however, the mechanisms underlying cisplatin-mediated nephrotoxicity are not fully understood. In this study, we investigated the role of anaphylatoxin C5a in the pathogenesis of cisplatin-mediated nephrotoxicity. Our data show that cisplatin-induced renal injury is significantly reduced in C5- or C5aR-deficient mice. However, pretreatment with C5 or C5a restores sensitivity to cisplatin-induced nephrotoxicity in C5-deficient mice. In wild-type mice, administration of cisplatin triggers the increased renal expression of multiple cytokines and caspases. This induction is diminished in C5-deficient mice, which is restored by pretreatment with C5 or C5a proteins. Interestingly, renal injury induced by cisplatin is similar between wild-type and CD59ab double knockout mice, and the formation of membrane attack complexes (MACs) by cisplatin in the kidney is diminished in C5-deficient mice, but not in C5aR-deficient mice. In conclusion, our findings suggest that C5a plays an important role in the pathogenesis of cisplatin nephrotoxicity. Likely, C5a binds to C5aR, leading to induction of proinflammatory cytokines and inflammation. The formation of MACs does not appear to contribute to the nephrotoxicity of cisplatin based on our study results.
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