Autophagy in cardiovascular biology

Abstract

Cardiovascular disease is the leading cause of death worldwide. As such, there is great interest in identifying novel mechanisms that govern the cardiovascular response to disease-related stress. First described in failing hearts, autophagy within the cardiovascular system has been widely characterized in cardiomyocytes, cardiac fibroblasts, endothelial cells, vascular smooth muscle cells, and macrophages. In all cases, a window of optimal autophagic activity appears to be critical to the maintenance of cardiovascular homeostasis and function; excessive or insufficient levels of autophagic flux can each contribute to heart disease pathogenesis. In this Review, we discuss the potential for targeting autophagy therapeutically and our vision for where this exciting biology may lead in the future.

Figure 2. Autophagy in the heart.

Autophagy is required for normal development of cardiac tissue and for cardiomyocyte terminal differentiation. Autophagy is also required for normal cardiac plasticity. Indeed, in the heart under normal conditions, autophagy plays a key role in regulating cardiomyocyte size as well as global cardiac structure and function. In the setting of disease, overactivation of autophagic flux can contribute to a transition to heart failure (HF).

Figure 1. Autophagy in the cardiovascular system.

Autophagic activity occurs in all cell types within the cardiovascular system. This activity contributes to a wide range of cellular events in normal physiology, growth, and development and in disease-related pathophysiology.