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        Activin/ myostatin receptor signaling and vascular calcifications in chronic kidney disease: A “liaison dangereuse”?

        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

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