Endurance under stress and cardioprotective functions by cardiac fibroblasts

Abstract

In the interstitium, the majority of cells are fibroblasts (1,2). Apoptosis or programmed cell death is an essential stage of cell cycle in cardiac morphogenesis during development and of central importance in maintaining homeostasis by eliminating the damaged and dysfunctional fibroblasts which will be replaced by new generation of cells. The mechanisms of apoptosis in cardiac fibroblasts are vastly unknown and in depth examination of various intracellular pathways responsible for apoptosis in response to environmental stress are yet to be performed. Relatively more is known on signals controlling apoptosis in cardiac myocytes than in cardiac fibroblasts. This issue is discussed in detail in separate chapter. Based on as yet limited information on both systems it is evident that the intracellular mechanisms and extracellular inducers of apoptosis in cardiac fibroblasts are not similar to those in post-mitotic cardiac myocytes. It is also evident that under environmental stress, such as hypoxia, which would cause apoptosis and cell death in cardiac myocytes, cardiac fibroblasts survive if not indefinitely, at least longer. This resilience lends support to the notion that cardiac fibroblasts may indeed have a mission to protect other cardiac cells or to compensate for their loss. In the past decade a growing body of evidence demonstrating various functions of cardiac fibroblasts has emerged and their role in the regulation of biological responses of other cardiac cells during development, normal growth, aging, ventricular hypertrophy and heart failure after myocardial infarction has been recognized.