Renal fibrosis is characterized by the proliferation of renal intrinsic cells, activation of renal interstitial fibroblasts and deposition of extracellular matrix (ECM), processes that lead to the progressive loss of renal function. Renal fibrosis is characterized by the proliferation of renal intrinsic cells, activation of renal interstitial fibroblasts, and septal fibrosis is recognized as a marker for the progression of chronic kidney disease, a condition that is associated with high morbidity and mortality and is a significant public health burden. Despite extensive studies, there are no effective treatments for renal fibrosis. Adiponectin (APN) is a protein mainly produced by adipocytes that has anti-inflammatory and anti-atherosclerotic effects, improves insulin resistance and provides other salutary effects. Recent studies found that APN can inhibit ECM deposition by inhibiting inflammation and oxidative stress, and by regulating the TGF-β, AMPK, MCP-1 and other signalling pathways. Many recent studies have examined the roles of these pathways in the pathogenesis of renal fibrosis. In this article, we review the pathogenic mechanism of APN in renal fibrosis and provide a theoretical basis for delaying and blocking renal fibrosis by alteration of APN activity.
Keywords: AMPK; TGF-β; adiponectin; chronic kidney disease; renal fibrosis.
© 2020 Asian Pacific Society of Nephrology.