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PRDM16 reduces cellular senescence by upregulating GSTM1

ABSTRACT: Cellular senescence is a hallmark of aging and the accumulation of senescent cells (SnCs) accelerates the aging process, contributing to aging-related organ disorders. The PRDF1 and RIZ1 homology domain (PRDM) protein exhibits robust transcriptional regulatory activities and governs a wide range of biological processes. However, its roles in cellular senescence remain unclear. Here, we demonstrated that PRDM16, a member of the PRDM protein family, decreased significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributed to cellular senescence in various organs, including the kidneys, heart, lungs, hippocampus, stomach, and gut, leading to accelerated aging-related organ injury. Furthermore, tubular-specific Prdm16 deletion aggravated irradiation-induced kidney aging and aging-related kidney diseases in irradiated mice subjected to ischemia-reperfusion surgery. Exogenous PRDM16 gene delivery by lentivirus effectively attenuated cellular senescence in vitro and in vivo. Mechanistically, PRDM16 improved glutathione metabolism and inhibited oxidative DNA damage, which is a driving force of senescence. Specifically, PRDM16 upregulated the transcription of glutathione S-transferase mu 1 (GSTM1) by binding to its promoter region. Transfection with GSTM1 reversed PRDM16 deficiency-induced cellular senescence and kidney aging. Collectively, our results provide a potential target for the investigation of anti-aging therapies.

ORGANISM(S): Mus musculus

PROVIDER: GSE307024 | GEO | 2025/09/02

REPOSITORIES: GEO

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PRDM16 restricts cellular senescence by upregulating GSTM1

Project description:Cellular senescence is a hallmark of aging, and the accumulation of senescent cells (SnCs) accelerates the aging process and contributes to aging-related organ disorders. The PRDMs exhibit robust transcriptional regulatory activity and govern a wide range of biological processes. However, the role of PRDMs in cellular senescence and aging remain unclear. Here, we have demonstrated that PRDM16, among PRDMs, is decreased significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributes to cellular senescence in various organs, including the kidney, heart, lung, brain hippocampus, stomach, and gut; subsequently leading to accelerated aging-related organ injury. Furthermore, tubular specific Prdm16 deletion aggravates irradiation induced kidney aging, and aging-related kidney disease subjected to ischemia reperfusion surgery. Exogenous PRDM16 gene delivery by lentivirus effectively attenuates cellular senescence in vitro and in vivo. Mechanistically, PRDM16 improves glutathione metabolism and inhibits oxidative DNA damage, the driving force of senescence. Especially, PRDM16 increases glutathione-S-transferase activity by upregulating the transcription of GSTM1. Transfection of GSTM1 restored cellular senescence and kidney aging caused by PRDM16 deficiency. Taken together, we provide a potential target for investigating the anti-aging therapy.

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