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Roberto Ferrari

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Francisco Fernández-AvilésJeroen BaxMichael BöhmThomas F. LüscherFrank Ruschitzka

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Healthy versus sick myocytes: metabolism, structure and function

R. Ferrari
DOI: http://dx.doi.org/10.1016/S1520-765X(02)90084-2 G1-G12 First published online: 1 November 2002

Abstract

The myocytes are extraordinary cells. They are immortal and contract for a lifetime, supporting the peripheral circulation. In order to do so, they have a unique ultrastructure and unique biochemical machinery that allows them to produce enough adenosine triphosphate to support the contraction. This article deals with the ultrastructure of cardiac muscle and myocytes, and with our current understanding of cardiac metabolism. In addition, the process of contraction is taken into consideration, as well as the mechanisms that allow the adult myocyte to be a terminal cell. However, even the myocytes can die; this can happen by necrosis as a result of an external insult (e.g. a lack of oxygen due to an abrupt occlusion of a coronary artery) or by apoptosis — a genetically programmed type of death that is operative in foetal life. Interestingly, and quite amazingly, under pathological conditions such as acute myocardial infarction or congestive heart failure, this genetic programme is reinstated and apoptosis can then occur, thus resembling features that occur un the embryonic phenotype. The metabolic alterations that occur under pathological conditions such as myocardial ischaemia are also addressed in depth, with several references to the so-called ‘new ischaemic syndromes’, such as stunning, hibernation and reperfusion paradox. The review is presented in light of an understanding of the biochemical and biomolecular changes that occur in pathological conditions, with the hope that this will provide room for innovative therapeutic intervention.

  • Apoptosis
  • contraction
  • heart failure
  • hypertrophy
  • metabolism
  • myocyte
  • necrosis
  • remodelling