title: Integrins and integrin-related proteins in cardiac fibrosis.
abstract: Cardiac fibrosis is one of the major components of the healing mechanism following any injury of the heart and as such may contribute to both systolic and diastolic dysfunction in a range of pathophysiologic conditions. Canonically, it can occur as part of the remodeling process that occurs following myocardial infarction or that follows as a response to pressure overload. Integrins are cell surface receptors which act in both cellular adhesion and signaling. Most importantly, in the context of the continuously contracting myocardium, they are recognized as mechanotransducers. They have been implicated in the development of fibrosis in several organs, including the heart. This review will focus on the involvement of integrins and integrin-related proteins, in cardiac fibrosis, outlining the roles of these proteins in the fibrotic responses in specific cardiac pathologies, discuss some of the common end effectors (angiotensin II, transforming growth factor beta 1 and mechanical stress) through which integrins function and finally discuss how manipulation of this set of proteins may lead to new treatments which could prove useful to alter the deleterious effects of cardiac fibrosis.
authors.affiliation: Department of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: chaochen@ucsd.edu.
authors.forename: Chao
authors.initials: C
authors.lastname: Chen
authors.affiliation: Department of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: rli@ucsd.edu.
authors.forename: Ruixia
authors.initials: R
authors.lastname: Li
authors.affiliation: Department of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: rross@ucsd.edu.
authors.forename: Robert S
authors.initials: RS
authors.lastname: Ross
authors.affiliation: Department of Medicine, Cardiology, UCSD School of Medicine, La Jolla, CA 92093-0613, USA; Veterans Administration San Diego Healthcare System, San Diego, CA 92161, USA. Electronic address: amanso@ucsd.edu.
authors.forename: Ana Maria
authors.initials: AM
authors.lastname: Manso
mesh_terms: D000367:Age Factors; D000375:Aging; D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure; D002352:Carrier Proteins / Q000378:metabolism*; D016207:Cytokines / Q000378:metabolism; D058065:Diabetic Cardiomyopathies / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D058750:Epithelial-Mesenchymal Transition; D005355:Fibrosis; D006801:Humans; D016023:Integrins / Q000378:metabolism*; D058990:Molecular Targeted Therapy; D009203:Myocardial Infarction / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology*; D011485:Protein Binding; D013314:Stress, Mechanical
chemical_list: D002352:Carrier Proteins; D016207:Cytokines; D016023:Integrins; D000804:Angiotensin II
keywords: Angiotensin; Fibrosis; Integrins; Mechanical stress; Myocardium; Transforming growth factor beta