ArticleCellular and molecular life sciences : CMLS2025
PRDM16 suppresses pyroptosis to attenuate the progression of AKI caused by rhabdomyolysis via upregulation of USP10.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Deubiquitinating enzymes in kidney diseases: Molecular mechanisms, pathological roles and therapeutic opportunities (Review).Molecular medicine reports · 2026Review
- PRDM16 as a Multifaceted Pharmacological Target in Kidney Diseases: From Epigenetic Mechanisms to Therapeutic Strategies.Pharmaceuticals (Basel, Switzerland) · 2026Review
- USP10 deubiquitinase: Physiological function, diseases and therapeutic target (Review).International journal of molecular medicine · 2026Review
- PRDM16 protects retinal ganglion cells from ischemia-reperfusion Injury by regulating the RPL5/p53 axis.Cellular and molecular life sciences : CMLS · 2026Article
- YOD1 drives acute kidney injury by deubiquitinating Bax and promoting apoptosis in tubular epithelial cells.Theranostics · 2026Article
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Previous studies have indicated that PRDM16 suppresses apoptosis and ferroptosis, thereby mitigating the development of AKI triggered by ischemia, cisplatin, and sepsis. Nevertheless, the exact function and control mechanisms of PRDM16 in rhabdomyolysis-induced AKI are not fully understood. In this investigation, PRDM16 was found to inhibit ferrous myoglobin-induced pyroptosis in Boston University mouse proximal tubule (BUMPT) cells. At the molecular level, PRDM16 binds to the USP10 promoter, enhancing its expression and subsequently inhibiting the NLRP3-Caspase1-GSDMD and Caspase3-GSDME pathways. Rhabdomyolysis-induced AKI was alleviated in PRDM16 KI mice, whereas PRDM16 KO exacerbated the condition. Furthermore, PNPs-encapsulated formononetin significantly attenuated the progression of rhabdomyolysis-induced AKI. In conclusion, PRDM16 suppresses pyroptosis and ameliorates rhabdomyolysis-induced AKI by regulating the USP10/NLRP3-Caspase1-GSDMD and Caspase3-GSDME pathways. PNPs-encapsulated formononetin emerges as a promising therapeutic strategy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.