Am J Physiol Heart Circ Physiol 315: H629–H631, 2018. First published June 1, 2018; doi:10.1152/ajpheart.00315.2018. EDITORIAL FOCUS LOXury of inhibiting ﬁbrosis in volume overload cardiomyopathy Sayantan Jana and Zamaneh Kassiri Department of Physiology, Cardiovascular Research Center, University of Alberta, Edmonton, Alberta, Canada Submitted 21 May 2018; accepted in ﬁnal form 29 May 2018 A central characteristic of various cardiomyopathies is adverse ﬁbrotic diseases and proposed as a biomarker for systemic structural remodeling of the myocardium and the extracellular sclerosis (6). Interstitial ﬁbrosis plays a critical role in determining myo- matrix (ECM). Hypertrophy is a common feature of myocar- cardial contractility and cardiac performance. LOX has been dial remodeling that is often associated with ﬁbrosis (adverse shown to be an important player in myocardial ﬁbrosis and ECM remodeling). In broad terms, two major causes of myo- heart failure (4). However, global deﬁciency of LOX is peri- cardial hypertrophy are pressure overload (PO) and volume natally lethal due to aortic aneurysm and possibly aortic rup- overload (VO). PO is an increase in afterload that can occur ture (5), which has limited the possibility of examining the secondary to hypertension or aortic stenosis and results in direct role of LOX in various
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Sep 1, 2018
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