<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Yuan Q</submitter><funding>Hubei Province Postdoctoral Innovative Talent Training Program</funding><funding>National Natural Science Foundation of China</funding><funding>Innovation and Development Joint Fund of Enshi</funding><funding>Key Research and Development Program of Hubei Province</funding><pagination>e01233</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12677672</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>12(45)</volume><pubmed_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, this work demonstrates that PRDM16, a member of the PRDM protein family, decreases significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributes 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 aggravates irradiat</pubmed_abstract><journal>Advanced science (Weinheim, Baden-Wurttemberg, Germany)</journal><pubmed_title>PRDM16 Reduces Cellular Senescence by Upregulating GSTM1.</pubmed_title><pmcid>PMC12677672</pmcid><funding_grant_id>82300851</funding_grant_id><funding_grant_id>82300843</funding_grant_id><funding_grant_id>2024HBBHCXB028</funding_grant_id><funding_grant_id>81974097</funding_grant_id><funding_grant_id>82300786</funding_grant_id><funding_grant_id>82100794</funding_grant_id><funding_grant_id>81800610</funding_grant_id><funding_grant_id>82470771</funding_grant_id><funding_grant_id>82200808</funding_grant_id><funding_grant_id>82370728</funding_grant_id><funding_grant_id>82100729</funding_grant_id><funding_grant_id>82170773</funding_grant_id><funding_grant_id>2023BCB034</funding_grant_id><funding_grant_id>82200841</funding_grant_id><funding_grant_id>2024AFD083</funding_grant_id><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Xie Y</pubmed_authors><pubmed_authors>Zhu Y</pubmed_authors><pubmed_authors>Yuan Q</pubmed_authors><pubmed_authors>Hu M</pubmed_authors><pubmed_authors>Tang B</pubmed_authors><pubmed_authors>Zhang C</pubmed_authors><pubmed_authors>Su H</pubmed_authors></additional><is_claimable>false</is_claimable><name>PRDM16 Reduces Cellular Senescence by Upregulating GSTM1.</name><description>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, this work demonstrates that PRDM16, a member of the PRDM protein family, decreases significantly in multiple organs of aged mice compared to young mice. Global Prdm16 deletion contributes 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 aggravates irradiat</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-05T22:24:29.275Z</modification><creation>2026-05-22T03:15:58.887Z</creation></dates><accession>S-EPMC12677672</accession><cross_references><pubmed>40946183</pubmed><doi>10.1002/advs.202501233</doi></cross_references></HashMap>