ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2020
MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- MYSM1 attenuates osteoarthritis by recruiting PP2A to deubiquitinate and dephosphorylate RIPK2.Bone research · 2025Article
- Deubiquitinase MYSM1 drives myocardial ischemia/reperfusion injury by stabilizing STAT1 in cardiomyocytes.Theranostics · 2025Article
- Acupotomy Ameliorates KOA Related Chondrocyte Premature Senescence Through YAP/FOXD1 Pathway.Journal of pain research · 2025Article
- Deubiquitinase MYSM1 promotes doxorubicin-induced cardiotoxicity by mediating TRIM21-ferroptosis axis in cardiomyocytes.Cell communication and signaling : CCS · 2024Article
- Deubiquitinase MYSM1: An Important Tissue Development and Function Regulator.International journal of molecular sciences · 2024Review
- Integrative analysis of the transcriptome and metabolome reveals the importance of hepatokine FGF21 in liver aging.Genes & diseases · 2024Article
- MYSM1 acts as a novel co-activator of ERα to confer antiestrogen resistance in breast cancer.EMBO molecular medicine · 2024Article
- Branched-Chain Amino Acid Accumulation Fuels the Senescence-Associated Secretory Phenotype.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Downregulation of Krüppel-like factor 14 accelerated cellular senescence and aging.Aging cell · 2023Article
- Genetic and Pharmacological Inhibition of Astrocytic Mysm1 Alleviates Depressive-Like Disorders by Promoting ATP Production.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Article
- MYSM1 Suppresses Cellular Senescence and the Aging Process to Prolong Lifespan.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is a universal feature of life that is a major focus of scientific research and a risk factor in many diseases. A comprehensive understanding of the cellular and molecular mechanisms of aging are critical to the prevention of diseases associated with the aging process. Here, it is shown that MYSM1 is a key suppressor of aging and aging-related pathologies. MYSM1 functionally represses cellular senescence and the aging process in human and mice primary cells and in mice organs. MYSM1 mechanistically attenuates the aging process by promoting DNA repair processes. Remarkably, MYSM1 deficiency facilitates the aging process and reduces lifespan, whereas MYSM1 over-expression attenuates the aging process and increases lifespan in mice. The functional role of MYSM1 is demonstrated in suppressing the aging process and prolonging lifespan. MYSM1 is a key suppressor of aging and may act as a potential agent for the prevention of aging and aging-associated diseases.
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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 OpenQuestion graph.