Molecular mechanisms underlying the transition of cardiac hypertrophy to heart failure.
Heart failure is a condition in which the heart cannot supply enough blood to the body's organs, and is a final common consequence of various heart diseases. In the past 2 decades, much progress has been made in understanding the molecular and cellular processes that contribute to cardiac hypertrophy and heart failure, leading to the development of effective therapies. However, heart failure remains a leading cause of mortality worldwide and the precise molecular mechanisms that mediate the transition of cardiac hypertrophy to heart failure are largely undefined. This review discusses the potential mechanisms of heart failure progression focusing on (1) cardiac myocyte loss, (2) abnormalities of calcium handling, and (3) myocardial ischemia and hypoxia. These factors are closely related, and are considered to contribute to the pathogenesis of contractile dysfunction and heart failure in a cooperative manner. Elucidation of the molecular mechanisms underlying the transition of cardiac hypertrophy to heart failure will lead to the development of novel therapeutic strategies for heart diseases.
Oka
Toru
T
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Japan.
Komuro
Issei
I
D001343:Autophagy; D002118:Calcium / Q000378:metabolism; D006332:Cardiomegaly / Q000150:complications*; D016923:Cell Death; D018450:Disease Progression; D050991:GATA4 Transcription Factor / Q000378:metabolism; D006333:Heart Failure / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D000860:Hypoxia / Q000150:complications; D017202:Myocardial Ischemia / Q000150:complications; D032383:Myocytes, Cardiac / Q000473:pathology; D009336:Necrosis; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D050991:GATA4 Transcription Factor; D042461:Vascular Endothelial Growth Factor A; D002118:Calcium