Caveolin-1 in the Pathogenesis of Diabetic Nephropathy: Potential Therapeutic Target?

• Published in: Current diabetes reports 2017-03, Vol.17 (3), p.19-19, Article 19
• Main Authors: Van Krieken, Richard, Krepinsky, Joan C.
• Format: Article
• Language: English
• Subjects: Animals; Caveolae - physiology; Caveolin 1 - antagonists & inhibitors; Caveolin 1 - physiology; Diabetes; Diabetic Nephropathies - drug therapy; Diabetic Nephropathies - etiology; Diabetic Nephropathies - physiopathology; Extracellular Matrix - metabolism; Humans; Medicine; Medicine & Public Health; Microvascular Complications—Nephropathy (M Afkarian; Oxidative Stress; Section Editor; Signal Transduction - physiology; Topical Collection on Microvascular Complications—Nephropathy
• ISSN: 1534-4827; 1539-0829
• DOI: 10.1007/s11892-017-0844-9

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.