Abstract
Diabetic nephropathy (DN) together with glomerular hyperfiltration has been implicated in the development of diabetic microangiopathy in the initial stage of diabetic diseases. Increased amounts of urinary protein in DN may be associated with functional and morphological alterations of podocyte, mainly including podocyte hypertrophy, epithelial-mesenchymal transdifferentiation (EMT), podocyte detachment, and podocyte apoptosis. Accumulating studies have revealed that disruption in multiple renal signaling pathways had been critical in the progression of these pathological damages, such as adenosine monophosphate-activated kinase signaling pathways (AMPK), wnt/β-catenin signaling pathways, endoplasmic reticulum stress-related signaling pathways, mammalian target of rapamycin (mTOR)/autophagy pathway, and Rho GTPases. In this review, we highlight new molecular insights underlying podocyte injury in the progression of DN, which offer new therapeutic targets to develop important renoprotective treatments for DN over the next decade.
Highlights
Diabetic nephropathy (DN), as the primary cause of endstage renal failure, is one of the most serious complications in diabetic patients, which develops in up to 30%– 40% of patients with types 1 or 2 diabetes mellitus [1]
Imasawa et al [8] declared that structure and function in podocyte molecules transformed in highglucose conditions, which resulted from suppression of myocyte-specific enhancer factor 2C (MEF2C) and myogenic factor 5 (MYF5) expressions through using a conditionally differentiating human podocyte cell line
Several studies suggested that mTORC1 was closely associated with the activation of podocyte hypertrophy which was induced by high glucose [13]
Summary
Diabetic nephropathy (DN), as the primary cause of endstage renal failure, is one of the most serious complications in diabetic patients, which develops in up to 30%– 40% of patients with types 1 or 2 diabetes mellitus [1]. An early sign of DN is an increased amount of urinary protein and characterized by mesangial nodular hyperplasia and thickening of the glomerular basement membrane (GBM). Microalbuminuria plays an important role in the change of the GBM. A detailed renal biopsy data analysis regarding diabetics showed that diabetic kidney damage would include visceral epithelial cells and sertoli cell dysfunction [2, 3]. Some researches demonstrated that podocyte injury had association with the development of DN [4], the mechanisms underlying this association are still not entirely understood and need to be further investigated
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