Extracellular matrix metabolism in diabetic nephropathy.

By R. M. Mason, N. Wahab. Journal of the American Society of Nephrology, 2003

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A Glimpse of Various Pathogenetic Mechanisms of Diabetic Nephropathy (2011, background): “Well-described characteristic glomerular changes include mesangial cell proliferation and hypertrophy, excessive accumulation of extracellular matrix (ECM) proteins in the form of increased mesangial matrix, and thickening of the glomerular basement membrane (GBM), which eventually leads to nodular ”
Oxidative stress and diabetic retinopathy: Molecular mechanisms, pathogenetic role and therapeutic implications (2020, background): “kines incurs the upregulation of ECM genes, fibrosis, and thicken CBMs ultimately [199].”
Diabetic Nephropathy: Mechanisms of Renal Disease Progression (2008, background): “They include hyperplasia/ hypertrophy of various cell types of the glomerulus and tubules, associated with thickening of glomerular and tubular basement membranes, and expansion of tubulo-interstitial and mesangial compartments (3).”
Endothelial progenitor cell dysfunction: a novel concept in the pathogenesis of vascular complications of type 1 diabetes. (2004, neutral): “Interestingly, many of these alterations have been reported to be associated with diabetes in general, hyperglycemia, or oxidative stress such as plasminogen activator inhibitor 1 (15) and osteopontin (16).”