title: The role of autophagy in cardiac hypertrophy.
abstract: Autophagy is conserved in nature from lower eukaryotes to mammals and is an important self-cannibalizing, degradative process that contributes to the elimination of superfluous materials. Cardiac hypertrophy is primarily characterized by excess protein synthesis, increased cardiomyocyte size, and thickened ventricular walls and is a major risk factor that promotes arrhythmia and heart failure. In recent years, cardiomyocyte autophagy has been considered to play a role in controlling the hypertrophic response. However, the beneficial or aggravating role of cardiomyocyte autophagy in cardiac hypertrophy remains controversial. The exact mechanism of cardiomyocyte autophagy in cardiac hypertrophy requires further study. In this review, we summarize the controversies associated with autophagy in cardiac hypertrophy and provide insights into the role of autophagy in the development of cardiac hypertrophy. We conclude that future studies should emphasize the relationship between autophagy and the different stages of cardiac hypertrophy, as well as the autophagic flux and selective autophagy. Autophagy will be a potential therapeutic target for cardiac hypertrophy.
authors.affiliation: Post-Doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China Hunan Children's Hospital and School of Pediatrics, University of South China, Changsha 410007, China.
authors.forename: Lanfang
authors.initials: L
authors.lastname: Li
authors.affiliation: Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang 421001, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Xu
authors.affiliation: Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang 421001, China.
authors.forename: Lu
authors.initials: L
authors.lastname: He
authors.affiliation: Post-Doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China Hunan Children's Hospital and School of Pediatrics, University of South China, Changsha 410007, China.
authors.forename: Lijun
authors.initials: L
authors.lastname: Peng
authors.affiliation: Post-Doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China.
authors.forename: Qiaoqing
authors.initials: Q
authors.lastname: Zhong
authors.affiliation: Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pharmacy and Pharmacology, Learning Key Laboratory for Pharmacoproteomics, University of South China, Hengyang 421001, China lxchen6@126.com z_sjiang@126.com.
authors.forename: Linxi
authors.initials: L
authors.lastname: Chen
authors.affiliation: Post-Doctoral Mobile Stations for Basic Medicine, Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerology of Hunan Province, University of South China, Hengyang 421001, China lxchen6@126.com z_sjiang@126.com.
authors.forename: Zhisheng
authors.initials: Z
authors.lastname: Jiang
mesh_terms: D000818:Animals; D001343:Autophagy / Q000502:physiology*; D006332:Cardiomegaly / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology*; D004195:Disease Models, Animal; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac / Q000473:pathology / Q000502:physiology; D015398:Signal Transduction
keywords: autophagic flux; autophagy; cardiac function; cardiac hypertrophy; cell signaling