ArticleActa pharmacologica Sinica2024
MDM2 accelerated renal senescence via ubiquitination and degradation of HDAC1.
Article in Acta pharmacologica Sinica, 2024. 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.
- From a Shared Stress to Cell-Type-Specific Responses: The Heterogeneous Mechanisms of High Glucose-Induced Cellular Senescence in Diabetic Kidney Disease.Journal of diabetes research · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
- 1,8-Cineole ameliorates vascular endothelial senescence in diabetes mellitus by directly targeting and deubiquitinating PPAR-γJournal of pharmaceutical analysis · 2025Article
- Exploring the pathophysiological relationship between bisphenol A exposure and ischemic stroke risk using network toxicology and machine learning.BMC neurology · 2025Article
- Immunoinflammation and post-translational modifications in the aging process.Journal of translational medicine · 2025Review
- Shenyuan granules improve cellular senescence through Klotho-mediated p16/p21 signaling pathway in diabetic kidney disease.Frontiers in medicine · 2025Article
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9 authors.
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Abstract
Senescence, an intricate and inevitable biological process, characterized by the gradual loss of homeostasis and declining organ functions. The pathological features of cellular senescence, including cell cycle arrest, metabolic disruptions, and the emergence of senescence-associated secretory phenotypes (SASP), collectively contribute to the intricate and multifaceted nature of senescence. Beyond its classical interaction with p53, murine double minute gene 2 (MDM2), traditionally known as an E3 ubiquitin ligase involved in protein degradation, plays a pivotal role in cellular processes governing senescence. Histone deacetylase (HDAC), a class of histone deacetylases mainly expressed in the nucleus, has emerged as a critical contributor to renal tissues senescence. In this study we investigated the interplay between MDM2 and HDAC1 in renal senescence. We established a natural aging model in mice over a 2-year period that was verified by SA-β-GAL staining and increased expression of senescence-associated markers such as p21, p16, and TNF-α in the kidneys. Furthermore, we showed that the expression of MDM2 was markedly increased, while HDAC1 expression underwent downregulation during renal senescence. This phenomenon was confirmed in H
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