LOXury of inhibiting fibrosis in volume overload cardiomyopathy

LOXury of inhibiting fibrosis in volume overload cardiomyopathy 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

LOXury of inhibiting fibrosis in volume overload cardiomyopathy

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ISSN
0363-6135
eISSN
1522-1539
D.O.I.
10.1152/ajpheart.00315.2018
Publisher site
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Abstract

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

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Sep 1, 2018

References

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