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Podocyte Autophagy: A Potential Therapeutic Target to Prevent the Progression of
Diabetic Nephropathy
#MMPMID28512641
Liu N
; Xu L
; Shi Y
; Zhuang S
J Diabetes Res
2017[]; 2017
(?): 3560238
PMID28512641
show ga
Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD),
becomes a worldwide problem. Ultrastructural changes of the glomerular filtration
barrier, especially the pathological changes of podocytes, lead to proteinuria in
patients with diabetes. Podocytes are major components of glomerular filtration
barrier, lining outside of the glomerular basement membrane (GBM) to maintain the
permeability of the GBM. Autophagy is a high conserved cellular process in
lysosomes including impaired protein, cell organelles, and other contents in the
cytoplasm. Recent studies suggest that activation of autophagy in podocytes may
be a potential therapy to prevent the progression of DN. Here, we review the
mechanisms of autophagy in podocytes and discuss the current studies about
alleviating proteinuria via activating podocyte autophagy.
|*Autophagy
[MESH]
|*Podocytes
[MESH]
|AMP-Activated Protein Kinases/metabolism
[MESH]
|Class I Phosphatidylinositol 3-Kinases/metabolism
[MESH]
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