The podocyte in diabetic kidney disease
#MMPMID19838599
Stitt-Cavanagh E
; MacLeod L
; Kennedy C
ScientificWorldJournal
2009[Oct]; 9
(?): 1127-39
PMID19838599
show ga
Approaching epidemic levels, diabetic kidney disease (DKD) is now the leading
cause of end-stage renal disease (ESRD). Microalbuminuria is an early clinical
marker of DKD that results from damage to the glomerular filtration barrier at
the level of the highly differentiated glomerular podocyte cells. Injury to these
epithelial cells, podocytopathies, includes cellular hypertrophy, foot process
effacement, detachment from the glomerular basement membrane, and apoptosis. Here
we review the role of a number of recently identified factors that contribute to
podocytopathies in DKD. These factors include members of the renin-angiotensin
system (RAS), including angiotensin-converting enzyme (ACE) types 1 and 2,
prorenin and its receptor, reactive oxygen species (ROS), prostanoids, peroxisome
proliferator-activated receptors (PPAR), advanced glycation end-products (AGEs)
and their receptors (RAGE), adiponectin, and microRNAs. As the number of
therapeutic options that slow, but do not halt, the progression of DKD to ESRD
remains limited, a more comprehensive understanding of the signaling events that
contribute to this increasingly prevalent disease may identify novel avenues for
treatment and prevention.
free
free
free
