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ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Review Article

Mechanosensing and Regulation of Cardiac Function

David E Dostal1,2*, Hao Feng2, Damir Nizamutdinov2, Honey B Golden2, Syeda H Afroze4, Joseph D Dostal2, John C Jacob2, Donald M Foster1, Carl Tong3, Shannon Glaser1,4 and Gerilechaogetu FNU2
1Central Texas Veterans Health Care System, Temple, Texas, USA
2Division of Molecular Cardiology, Cardiovascular Research Institute, Texas A&M University Health Science Centre, College of Medicine, Temple, Texas, USA
3Systems Biology and Translational Medicine, the Texas A&M University Health Science Centre, College of Medicine, Temple, Texas, USA
4Scott & White Healthcare - Digestive Disease Research Centre, Temple, Texas, USA
Corresponding Author : David E Dostal
Central Texas Veterans Health Care System
Division of Molecular Cardiology, Department of Internal Medicine
Cardiovascular Research Institute
The Texas A&M University Health Science Centre
1901 South 1st Street, Bldg. 205, Temple TX 76504, USA
Tel: 254-743-2464
Fax: 254-743-0165
E-mail: [email protected]
Received March 24, 2014; Accepted May 22, 2014; Published June 05, 2014
Citation: Dostal DE, Feng H, Nizamutdinov D, Golden HB, Afroze SH, et al. (2014) Mechanosensing and Regulation of Cardiac Function. J Clin Exp Cardiolog 5:314. doi:10.4172/2155-9880.1000314
Copyright: © 2014 Dostal DE, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

The role of mechanical force as an important regulator of structure and function of mammalian cells, tissues, and organs has recently been recognized. However, mechanical overload is a pathogenesis or comorbidity existing in a variety of heart diseases, such as hypertension, aortic regurgitation and myocardial infarction. Physical stimuli sensed by cells are transmitted through intracellular signal transduction pathways resulting in altered physiological responses or pathological conditions. Emerging evidence from experimental studies indicate that β1-integrin and the angiotensin II type I (AT1) receptor play critical roles as mechanosensors in the regulation of heart contraction, growth and leading to heart failure. Integrin link the extracellular matrix and the intracellular cytoskeleton to initiate the mechanical signalling, whereas, the AT1 receptor could be activated by mechanical stress through an angiotensin-II-independent mechanism. Recent studies show that both Integrin and AT1 receptor and their downstream signalling factors including MAPKs, AKT, FAK, ILK and GTPase regulate heart function in cardiac myocytes. In this review we describe the role of mechanical sensors residing within the plasma membrane, mechanical sensor induced downstream signalling factors and its potential roles in cardiac contraction and growth.

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