ABSTRACT
Cells of the adult heart have, at the very least, limited potential for replication, yet these same cells must endure for an individual’s lifespan and respond to the range of physiological and pathological stresses that can occur during that time. The adaptations cardiomyocytes undergo in response to stress are well described, and include changes in cell size and shape, alterations in the composition of the contractile apparatus, remodeling of electrical components, and upregulation of protective mechanisms. All of these adaptations must occur while individual cardiomyocytes continue to participate in the mechanical events of cardiac contraction and relaxation. Although signaling mechanisms, transcriptional events, and electrical activities that regulate cardiomyocyte function are well known, it must be kept in mind that cardiomyocytes respond to more mechanical wear and tear than any other organ, and must also be able to ‘change out’ proteins during the course of phenotypic adaptation during normal development, and in response to hemodynamic changes. Cardiomyocytes must fold large, structurally complicated molecules appropriately to form the contractile apparatus, and must also degrade these proteins when necessary to maintain appropriate homeostasis. Disorder of these events can have devastating consequences for cardiac contractile function. In this chapter, the events that regulate protein folding and degradation are reviewed, bearing in mind the relationship these events have to regulation of cardiac structure, cell size and the response to injury.
