Dissemin is shutting down on January 1st, 2025

Published in

Springer (part of Springer Nature), Basic Research in Cardiology, 3(103), p. 228-231

DOI: 10.1007/s00395-008-0698-z

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Heart spotting.

Journal article published in 2008 by Hamid el Azzouzi, H. el Azzouzi, L. J. de Windt ORCID
This paper was not found in any repository, but could be made available legally by the author.
This paper was not found in any repository, but could be made available legally by the author.

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Abstract

Cardiac function depends upon several factors, including adequate cellular mass, intact contractile machinery, and adequate production of ATP. An appropriate homeostasis on all these levels is crucial for the daunting life-long task the myocardium faces. Not surprisingly, many alterations in the above factors have been spotted when the heart fails and hypothesized to play a causal role in the genesis of the failing heart. Indeed, development of cardiac hypertrophy and failure is associated with chamber remodeling as well as with changes of the phenotype at the level of the individual myocyte. Disturbed energy metabolism with impaired fatty acid oxidation and lower expression of proteins involved in ATP synthesis occurs during myocardial hypertrophy and heart failure. The altered expression of proteins from metabolic pathways may reflect mitochondrial dysfunction as a feature of the transition from compensated myocardial hypertrophy with preserved fatty acid metabolism to impaired energy metabolism in heart failure. ; Cardiac function depends upon several factors, including adequate cellular mass, intact contractile machinery, and adequate production of ATP. An appropriate homeostasis on all these levels is crucial for the daunting life-long task the myocardium faces. Not surprisingly, many alterations in the above factors have been spotted when the heart fails and hypothesized to play a causal role in the genesis of the failing heart. Indeed, development of cardiac hypertrophy and failure is associated with chamber remodeling as well as with changes of the phenotype at the level of the individual myocyte. Disturbed energy metabolism with impaired fatty acid oxidation and lower expression of proteins involved in ATP synthesis occurs during myocardial hypertrophy and heart failure. The altered expression of proteins from metabolic pathways may reflect mitochondrial dysfunction as a feature of the transition from compensated myocardial hypertrophy with preserved fatty acid metabolism to impaired energy metabolism in heart failure.