Uticaj fosfolipaze C u norepinefrinom izazvan hipertrofični odgovor kardiomiocita

Phospholipase C in Cardiac Hypertrophy

  • Paramjit S Tappia Asper Clinical Research Institute, St. Boniface Hospital Research
  • Vijayan Elimban Institute of Cardiovascular Sciences & Department of Physiology & Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba
  • Naranjan S Dhalla 2Institute of Cardiovascular Sciences & Department of Physiology & Pathophysiology, Max Rady College of Medicine, Rady Faculty of Health Sciences, University of Manitoba

Sažetak


Norepinephrine (NE) is known to mediate cardiomyocyte hypertrophy through the G protein coupled α1
-adrenoceptor (α1-AR) and the activation of the phosphoinositide-specific phospholipase C (PLC). Since the by-products of PLC activity are important downstream signal transducers for cardiac hypertrophy, the role
of and the regulatory mechanisms involved in the activation of PLC isozymes in cardiac hypertrophy are highlighted in this review. The discussion is focused to underscore PLC in different experimental models of cardiac hypertrophy, as well as in isolated adult and neonatal cardiomyocytes treated with NE. Particular
emphasis is laid concerning the α1-AR-PLC-mediated hypertrophic signalling pathway. From the information provided, it is evident that the specific activation of PLC isozymes is a primary signalling event in the α1
-AR mediated response to NE as well as initiation and progression of cardiac hypertrophy. Furthermore,
the possibility of PLC involvement in the perpetuation of cardiac hypertrophy is also described. It is suggested that specific PLC isozymes may serve as viable targets for the prevention of cardiac hypertrophy in patient population at-risk for the development of heart failure.

Biografija autora

Paramjit S Tappia, Asper Clinical Research Institute, St. Boniface Hospital Research
Asper Clinical Research Institute, Clinical Research Scientist

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Objavljeno
2022/06/29
Rubrika
Review article