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. Author manuscript; available in PMC: 2013 Mar 25.
Published in final edited form as: Curr Opin Cardiol. 2011 May;26(3):216–222. doi: 10.1097/HCO.0b013e328345980a

Figure 1. Schematic of autophagy pathways.

Figure 1

A variety of stimuli, including both physiological (e.g., starvation) and pathologic stresses, trigger cardiac autophagy. The first step in the process is nucleation. Classically, a complex composed of class III PI3K and Beclin 1 complex is involved. This complex initiates formation of an isolated double membrane and subsequent membrane elongation. The membrane then fuses upon itself, forming the distinctive double-membrane autophagosome. During the following fusion step, autophagosomes ultimately fuse with lysosomes, culminating in cargo degradation. The end-products of autolysosome cargo degradation provide both fuel and elemental building blocks to preserve vital cellular functions and remove toxic cellular elements. ATG, autophagy-related genes; PI3K-III, class III phosphatidylinositide-3-kinase; Vps34, vacuolar protein sorting 34.