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Am J Physiol Renal Physiol 297: F244-F256, 2009. First published March 11, 2009; doi:10.1152/ajprenal.00033.2009
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REVIEW

Autophagy: molecular machinery, regulation, and implications for renal pathophysiology

Sudharsan Periyasamy-Thandavan, Man Jiang, Patricia Schoenlein, and Zheng Dong

Department of Cellular Biology and Anatomy, Medical College of Georgia and Charlie Norwood Department of Veterans Affairs Medical Center, Augusta, Georgia

Submitted 22 January 2009 ; accepted in final form 5 March 2009

ABSTRACT

Autophagy is a cellular process of "self-eating." During autophagy, a portion of cytoplasm is enveloped in double membrane-bound structures called autophagosomes, which undergo maturation and fusion with lysosomes for degradation. At the core of the molecular machinery of autophagy is a specific family of genes or proteins called Atg. Originally identified in yeast, Atg orthologs are now being discovered in mammalian cells and have been shown to play critical roles in autophagy. Traditionally, autophagy is recognized as a cellular response to nutrient deprivation or starvation whereby cells digest cytoplasmic organelles and macromolecules to recycle nutrients for self-support. However, studies during the last few years have indicated that autophagy is a general cellular response to stress. Interestingly, depending on experimental conditions, especially stress levels, autophagy can directly induce cell death or act as a mechanism of cell survival. In this review, we discuss the molecular machinery, regulation, and function of autophagy. In addition, we analyze the recent findings of autophagy in renal systems and its possible role in renal pathophysiology.

apoptosis; Atg; cytoprotection; mammalian target of rapamycin; phosphatidylinositol 3-kinase


Address for reprint requests and other correspondence: Z. Dong, Dept. of Cellular Biology and Anatomy, Medical College of Georgia, 1459 Laney Walker Blvd., Augusta, GA 30912 (e-mail: zdong{at}mail.mcg.edu)






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