Implications of autophagy for glomerular aging and disease

被引：49

作者：

Weide, Thomas ^{[2
,4
]}

Huber, Tobias B. ^{[1
,3
]}

机构：

[1] Univ Hosp Freiburg, Div Renal, D-79106 Freiburg, Germany

[2] Univ Hosp Muenster, Div Mol Nephrol, Munster, Germany

[3] Univ Freiburg, Ctr Biol Signalling Studies Bioss, Freiburg, Germany

[4] Univ Hosp Muenster, Div Mol Nephrol, Dept Internal Med D, D-48149 Munster, Germany

来源：

CELL AND TISSUE RESEARCH | 2011年 / 343卷 / 03期

关键词：

Autophagy; Glomerular; Aging; Disease; Renal function; PHOSPHATIDYLINOSITOL 3,5-BISPHOSPHATE; PODOCYTE NUMBER; MOUSE MODELS; NEURODEGENERATION; MICE; MEMBRANE; GLOMERULOSCLEROSIS; PHOSPHOINOSITIDES; DIFFERENTIATION; TRAFFICKING;

D O I：

10.1007/s00441-010-1115-0

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Glomerular diseases lead to a progressive decline in renal function and account for the vast majority of end-stage kidney diseases. Injury and loss of glomerular podocytes are common determining factors of glomerular disease progression and renal failure. Podocytes are a primary glomerular target of toxic, immune, metabolic, and oxidant stress, but little is known of the factors that counteract cellular stress signaling pathways. This review focuses on recent findings that identify autophagy as a critical homeostatic and quality control mechanism maintaining glomerular homeostasis.

引用

页码：467 / 473

页数：7

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