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

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

Research output: Contribution to journalReview article

110 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)F244-F256
JournalAmerican Journal of Physiology - Renal Physiology
Volume297
Issue number2
DOIs
StatePublished - Aug 1 2009

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Keywords

  • Apoptosis
  • Atg
  • Cytoprotection
  • Mammalian target of rapamycin
  • Phosphatidylinositol 3-kinase

ASJC Scopus subject areas

  • Physiology
  • Urology

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