Cardiac autophagy: good with the bad

Abstract

Stress-induced hypertrophic growth of the myocardium is a pathogenetic milestone in the progression of heart failure. Some evidence suggests that suppression of pathological cardiac hypertrophy per se is a viable target for therapeutic intervention, and cardiomyocyte autophagy is an attractive mechanism for consideration as a means of controlling the hypertrophic response. However, although considerable insights have been gleaned in the molecular mechanisms governing cardiomyocyte autophagy, many details critical to rational targeting of the response remain unknown. Among them, mechanisms underlying the adaptive and maladaptive features of autophagy are obscure. With time and further study, it is possible that this near-ubiquitous cardiac response to stress will emerge as a target for therapeutic manipulation.

Figure. Cardiomyocyte autophagy varies in response to different conditions

Basal autophagy is necessary for normal homeostasis of the cardiomyocyte. In response to pathological stress, autophagy may be adaptive in allowing for cardiomyocyte survival. Under severe or persistent stress, autophagy can be maladaptive, facilitating detrimental remodeling.