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2015 ; 11
(7
): 1130-45
Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Endothelial cell and podocyte autophagy synergistically protect from
diabetes-induced glomerulosclerosis
#MMPMID26039325
Lenoir O
; Jasiek M
; Hénique C
; Guyonnet L
; Hartleben B
; Bork T
; Chipont A
; Flosseau K
; Bensaada I
; Schmitt A
; Massé JM
; Souyri M
; Huber TB
; Tharaux PL
Autophagy
2015[]; 11
(7
): 1130-45
PMID26039325
show ga
The glomerulus is a highly specialized capillary tuft, which under pressure
filters large amounts of water and small solutes into the urinary space, while
retaining albumin and large proteins. The glomerular filtration barrier (GFB) is
a highly specialized filtration interface between blood and urine that is highly
permeable to small and midsized solutes in plasma but relatively impermeable to
macromolecules such as albumin. The integrity of the GFB is maintained by
molecular interplay between its 3 layers: the glomerular endothelium, the
glomerular basement membrane and podocytes, which are highly specialized
postmitotic pericytes forming the outer part of the GFB. Abnormalities of
glomerular ultrafiltration lead to the loss of proteins in urine and progressive
renal insufficiency, underlining the importance of the GFB. Indeed, albuminuria
is strongly predictive of the course of chronic nephropathies especially that of
diabetic nephropathy (DN), a leading cause of renal insufficiency. We found that
high glucose concentrations promote autophagy flux in podocyte cultures and that
the abundance of LC3B II in podocytes is high in diabetic mice. Deletion of Atg5
specifically in podocytes resulted in accelerated diabetes-induced podocytopathy
with a leaky GFB and glomerulosclerosis. Strikingly, genetic alteration of
autophagy on the other side of the GFB involving the endothelial-specific
deletion of Atg5 also resulted in capillary rarefaction and accelerated DN. Thus
autophagy is a key protective mechanism on both cellular layers of the GFB
suggesting autophagy as a promising new therapeutic strategy for DN.
|*Autophagy/drug effects
[MESH]
|Animals
[MESH]
|Apoptosis/drug effects
[MESH]
|Autophagy-Related Protein 5
[MESH]
|Cells, Cultured
[MESH]
|Diabetic Nephropathies/*pathology/physiopathology/*prevention & control
[MESH]
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