Abstract
Renal fibrosis is an inevitable consequence of parenchymal scarring and is the common final pathway that mediates almost all progressive renal diseases. Adiponectin, a hormone produced by adipose tissue, possesses potent anti-insulin, anti-inflammatory, and anti-fibrotic properties. Reportedly, adiponectin serves as an important messenger that facilitates complex interactions between adipose tissue and other metabolically related organs. In recent years, a growing body of evidence supports adiponectin involvement in renal fibrosis. These studies provide a deeper understanding of the molecular mechanism of action of adiponectin in renal fibrosis and also offer a potential preventive and therapeutic target for renal fibrosis. In this review, the physiological role of adiponectin is briefly introduced, and then the mechanism of adiponectin-mediated renal fibrosis and the related signaling pathways are described. Finally, we summarize the findings regarding the clinical value of adiponectin in renal fibrotic diseases and prospected its application potential.
Highlights
Chronic kidney disease (CKD) is a growing public health issue worldwide with an annual increase in incidence
Inflammation, oxidative stress, cytokine and signaling cascades, as well as fibroblast proliferation and activation constitute multifactorial etiopathogenetic contributors to renal fibrosis [2,3,4]. These aforementioned pathophysiological processes lead to hyperadiponectinemia that is associated with renal fibrosis in various presentations of CKD, its exact mechanism of action remains unclear [5, 6]
We summarize the recent findings regarding the role of adiponectin in renal fibrosis and update the current comprehensive knowledge regarding the usefulness of adiponectin-based treatments in renal fibrosis disease
Summary
Chronic kidney disease (CKD) is a growing public health issue worldwide with an annual increase in incidence. Based on in vitro experiments, Sajjad Esmaeili et al confirmed that APN reduces oxidative stress and associated kidney cell injury by inhibiting mTOR [33]. Several studies have confirmed the role of the APN-mediated AMPK signaling pathway in renal fibrosis. Fang et al reported that the APN signaling pathway regulates oxidative stress, podocyte foot fusion and the onset of proteinuria through in vivo and in vitro actions of AMPK [38].
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