title: Cardiomyocyte apoptosis in animal models of obesity.
abstract: Cardiovascular disease caused less than 10% of deaths worldwide at the beginning of the 20th century but accounted for nearly 50% toward its end. Obesity has seen a similarly sharp increase in prevalence and is a major contributing factor to the rise in cardiovascular disease incidence. Mechanisms of obesity-induced heart disease are multifaceted and remain largely unknown, but cardiomyocyte programmed cell death, or apoptosis, seems to play a critical role in their development and progression. The heart maintains a delicate balance between cell proliferation and cell death throughout its lifetime. Even a slight increase in the rate of myocyte apoptosis, as seen in various animal models, has devastating consequences for the heart. This article critically reviews studies conducted in animal models of obesity that have expanded our understanding of the mechanisms of cardiomyocyte apoptosis and their role in various obesity-associated cardiovascular diseases.
authors.affiliation: Division of Cardiology, Johns Hopkins University, Baltimore, MD 21205, USA.
authors.forename: Premal S
authors.initials: PS
authors.lastname: Trivedi
authors.forename: Lili A
authors.initials: LA
authors.lastname: Barouch
mesh_terms: D000818:Animals; D017209:Apoptosis; D002318:Cardiovascular Diseases / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D004195:Disease Models, Animal; D007333:Insulin Resistance; D020738:Leptin / Q000378:metabolism*; D008297:Male; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology*; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011924:Rats, Zucker; D012307:Risk Factors; D012680:Sensitivity and Specificity; D015398:Signal Transduction; D015996:Survival Rate
chemical_list: D020738:Leptin