Remodelling of the Myocyte at a Molecular Level — Relationship Between Myosin Isoenzyme Population and Sarcoplasmic Reticulum

Abstract

There is increasing evidence that the molecular structure of the myocyte is variable, critically depending on the functional load to which the heart is subjected on a long-term basis. The potential of the myocyte to adapt its functionally important structural elements to a given load represents an important means by which the heart can cope with a variety of loads ranging from those arising during physical exercise or increased blood pressure (1). Although such remodelling of the myocyte is of great functional relevance, only little is known at present in terms of the trigger reactions involved at the cellular or molecular level. In view of the great number of variable elements of the myocyte, it is unlikely that for each one there is a selective trigger signal. Rather, it can be assumed that a given stimulus affects a number of functionally coherent structures of the myocyte in a concerted manner. An understanding of mechanisms involved in the remodelling is the prerequisite not only for a rational description of myocardial performance but also for tracing the causes of pathological processes such as decompensation of the pressure loaded heart issuing in pump failure.