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Giacomo Garibotto,Pasquale Esposito,Daniela Picciotto,Daniela Verzola 대한신장학회 2019 Kidney Research and Clinical Practice Vol.38 No.4
Both myostatin (MSTN) and activin A, two peptide members of the transforming growth factor (TGF)-β super family, have been suggested to play major roles in complications of chronic kidney disease (CKD), including vascular and bone disease. Both MSTN and activin A share many similarities in terms of structure, signaling pathway, and functions with TGF-β, and have been initially studied as players in muscle cachexia in CKD and several other chronic diseases [1]. However, the last few years have witnessed a paradigm shift with respect to our understanding of the effects of MSTN/activin signaling in organs distant from muscle. There is ever-increasing evidence that the MSTN/activin pathway impacts the heart, arterial vessels, insulin sensitivity and vascular remodeling [2]. In addition, recent observations strongly suggest that activin A signaling plays a major role in the progression of kidney disease and CKD/mineral bone disorder (MBD) [2]. These “off target” actions of MSTN and activin A might contribute substantially to the pathophysiology of wasting, inflammation, vascular damage, and possibly progressive renal dysfunction in CKD