title: Regulation of apoptosis by angiotensin II in the heart and lungs (Review).
abstract: Cell death by apoptosis is now known to be an important mechanism of cell population control in organ development and in normal tissue homeostasis. Inappropriate apoptosis also contributes to the pathogenesis of a number of diseases involving the heart and lungs. Knowledge of the regulation of apoptosis in these organs is therefore of fundamental importance. A growing body of evidence suggests that the renin-angiotensin system (RAS), traditionally viewed as an endocrine system in the regulation of blood pressure, also functions as a regulator of apoptosis in a variety of cell types through both paracrine and autocrine mechanisms that are likely independent of the endocrine RAS. Much of the evidence in support of this premise comes from investigations of cardiac myocytes, endothelial cells and epithelial cells of the lung, both in culture and in situ within human pathological specimens and animal models of heart, vascular and pulmonary disease. Evidence from each of these areas is reviewed and discussed in relation to diseases of the heart, vascular system and lungs.
authors.affiliation: Second Division of Cardiology, Evangelismos General Hospital, Athens, Greece.
authors.forename: G
authors.initials: G
authors.lastname: Filippatos
authors.forename: M
authors.initials: M
authors.lastname: Tilak
authors.forename: H
authors.initials: H
authors.lastname: Pinillos
authors.forename: B D
authors.initials: BD
authors.lastname: Uhal
mesh_terms: D000804:Angiotensin II / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism; D006331:Heart Diseases / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008168:Lung / Q000166:cytology* / Q000378:metabolism; D008171:Lung Diseases / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000166:cytology* / Q000378:metabolism; D012084:Renin-Angiotensin System
chemical_list: D000804:Angiotensin II