Atrophied cardiomyocytes and their potential for rescue and recovery of ventricular function
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- 作者：Mark R. Heckle ; David M. Flatt ; Yao Sun ; Salvatore Mancarella…
- 关键词：Myocyte atrophy ; Oxidative stress ; Ubiquitin ligases ; Deiodinase ; 3 ; Angiotensin II ; Low intracellular T3 ; Rebuilding myocardium
- 刊名：Heart Failure Reviews
- 出版年：2016
- 出版时间：March 2016
- 年：2016
- 卷：21
- 期：2
- 页码：191-198
- 全文大小：651 KB
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David M. Flatt (2)
Yao Sun (2)
Salvatore Mancarella (3)
Tony N. Marion (4)
Ivan C. Gerling (5)
Karl T. Weber (2)
1. Department of Medicine, University of Tennessee Health Science Center, Memphis, TN, USA
2. Division of Cardiovascular Diseases, University of Tennessee Health Science Center, 956 Court Ave., Suite A312, Memphis, TN, 38163, USA
3. Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
4. Department of Microbiology, Immunology and Biochemistry, University of Tennessee Health Science Center, Memphis, TN, USA
5. Division of Endocrinology, University of Tennessee Health Science Center, Memphis, TN, USA - 刊物类别：Medicine
- 刊物主题：Medicine & Public Health
Cardiology - 出版者：Springer Netherlands
- ISSN：1573-7322
文摘
Cardiomyocytes must be responsive to demands placed on the heart’s contractile work as a muscular pump. In turn, myocyte size is largely dependent on the workload they perform. Both hypertrophied and atrophic myocytes are found in the normal and diseased ventricle. Individual myocytes become atrophic when encumbered by fibrillar collagen, such as occurs at sites of fibrosis. The mechanisms include: (a) being immobilized and subject to disuse with ensuing protein degradation mediated by redox-sensitive, proteolytic ligases of the ubiquitin–proteasome system and (b) dedifferentiated re-expressing fetal genes induced by low intracellular triiodothyronine (T3) via thyroid hormone receptor β1. This myocyte-selective, low T3 state is a consequence of heterocellular signaling emanating from juxtaposed scar tissue myofibroblasts and their secretome with its de novo generation of angiotensin II. In a paracrine manner, angiotensin II promotes myocyte Ca2+ entry and subsequent Ca2+ overload with ensuing oxidative stress that overwhelms antioxidant defenses to activate deiodinase-3 and its enzymatic degradation of T3. In the failing heart, atrophic myocytes represent an endogenous population of viable myocytes which could be rescued to augment contractile mass, reduce systolic wall stress (afterload) and recover ventricular function. Experimental studies have shown the potential for the rescue and recovery of atrophic myocytes in rebuilding the myocardium—a method complementary to today’s quest in regenerating myocardium using progenitor cells.