{"title":"应激心脏中PGC-1α和GDF15的相互作用。","authors":"Rong Tian","doi":"10.1038/s44161-025-00729-8","DOIUrl":null,"url":null,"abstract":"Upregulation of PGC-1α in the mouse heart during exercise training maintains mitochondrial homeostasis and promotes physiological hypertrophy by suppressing the stress-induced production of GDF15 in cardiomyocytes independently of its circulating levels. Identification of this cell-autonomous signaling circuit provides novel insights into the functional role of GDF15 in health and diseases. Future studies are warranted to investigate the interaction of PGC-1α and GDF15 in other stress conditions and in human subjects.","PeriodicalId":74245,"journal":{"name":"Nature cardiovascular research","volume":"4 10","pages":"1216-1218"},"PeriodicalIF":10.8000,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Interaction of PGC-1α and GDF15 in the stressed heart\",\"authors\":\"Rong Tian\",\"doi\":\"10.1038/s44161-025-00729-8\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Upregulation of PGC-1α in the mouse heart during exercise training maintains mitochondrial homeostasis and promotes physiological hypertrophy by suppressing the stress-induced production of GDF15 in cardiomyocytes independently of its circulating levels. Identification of this cell-autonomous signaling circuit provides novel insights into the functional role of GDF15 in health and diseases. Future studies are warranted to investigate the interaction of PGC-1α and GDF15 in other stress conditions and in human subjects.\",\"PeriodicalId\":74245,\"journal\":{\"name\":\"Nature cardiovascular research\",\"volume\":\"4 10\",\"pages\":\"1216-1218\"},\"PeriodicalIF\":10.8000,\"publicationDate\":\"2025-09-26\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nature cardiovascular research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://www.nature.com/articles/s44161-025-00729-8\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"CARDIAC & CARDIOVASCULAR SYSTEMS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature cardiovascular research","FirstCategoryId":"1085","ListUrlMain":"https://www.nature.com/articles/s44161-025-00729-8","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
Interaction of PGC-1α and GDF15 in the stressed heart
Upregulation of PGC-1α in the mouse heart during exercise training maintains mitochondrial homeostasis and promotes physiological hypertrophy by suppressing the stress-induced production of GDF15 in cardiomyocytes independently of its circulating levels. Identification of this cell-autonomous signaling circuit provides novel insights into the functional role of GDF15 in health and diseases. Future studies are warranted to investigate the interaction of PGC-1α and GDF15 in other stress conditions and in human subjects.