TY - JOUR
T1 - Autophagy
T2 - Molecular machinery, regulation, and implications for renal pathophysiology
AU - Periyasamy-Thandavan, Sudharsan
AU - Jiang, Man
AU - Schoenlein, Patricia
AU - Dong, Zheng
PY - 2009/8
Y1 - 2009/8
N2 - 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.
AB - 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.
KW - Apoptosis
KW - Atg
KW - Cytoprotection
KW - Mammalian target of rapamycin
KW - Phosphatidylinositol 3-kinase
UR - http://www.scopus.com/inward/record.url?scp=68049104247&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=68049104247&partnerID=8YFLogxK
U2 - 10.1152/ajprenal.00033.2009
DO - 10.1152/ajprenal.00033.2009
M3 - Review article
C2 - 19279132
AN - SCOPUS:68049104247
SN - 0363-6127
VL - 297
SP - F244-F256
JO - American Journal of Physiology - Renal Physiology
JF - American Journal of Physiology - Renal Physiology
IS - 2
ER -