Erschienen in:
01.03.2017 | Microvascular Complications—Nephropathy (M Afkarian, Section Editor)
Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?
verfasst von:
Richard Van Krieken, Joan C. Krepinsky
Erschienen in:
Current Diabetes Reports
|
Ausgabe 3/2017
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Abstract
Purpose of review
Diabetic nephropathy, a major microvascular complication of diabetes and the most common cause of end-stage renal disease, is characterized by prominent accumulation of extracellular matrix. The membrane microdomains caveolae, and their integral protein caveolin-1, play critical roles in the regulation of signal transduction. In this review we discuss current knowledge of the contribution of caveolin-1/caveolae to profibrotic signaling and the pathogenesis of diabetic kidney disease, and assess its potential as a therapeutic target.
Recent findings
Caveolin (cav)-1 is key to facilitating profibrotic signal transduction induced by several stimuli known to be pathogenic in diabetic nephropathy, including the most prominent factors hyperglycemia and angiotensin II. Phosphorylation of cav-1 on Y14 is an important regulator of these responses. In vivo studies support a pathogenic role for caveolae in the progression of diabetic nephropathy.
Summary
Targeting caveolin-1/caveolae would enable inhibition of multiple profibrotic pathways, representing a novel and potentially potent therapeutic option for diabetic nephropathy.