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Published on: May 2, 2025
Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?
Richard Van Krieken1, Joan C Krepinsky2
1Department of Medicine, Division of Nephrology, St. Joseph's Hospital, McMaster University, 50 Charlton Ave E, T3311, Hamilton, ON, L8N 4A6, Canada.
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. Targeting caveolin-1/caveolae would enable inhibition of multiple profibrotic pathways, representing a novel and potentially potent therapeutic option for diabetic nephropathy.
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