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?Klotho and Vascular Calcification: An Evolving Paradigm #MMPMID24867676
Hu MC; Kuro-o M; Moe OW
Curr Opin Nephrol Hypertens 2014[Jul]; 23 (4): 331-9 PMID24867676show ga
Purpose of Review: Cardiovascular disease remains the single most serious contributor to mortality in chronic kidney disease (CKD). Although conventional risk factors are prevalent in CKD, both cardiomyopathy and vasculopathy can be caused by pathophysiologic mechanisms specific to the uremic state. CKD is a state of systemic ?Klotho deficiency. While the molecular mechanism of action of ?Klotho is not well understood, the downstream targets and biologic functions of ?Klotho are astonishingly pleiotropic. An emerging body of literature links ?Klotho to uremic vasculopathy. Recent Findings: The expression of ?Klotho in the vasculature is controversial due to conflicting data. Regardless of whether ?Klotho acts a circulating or resident protein, there are good data associating changes in ?Klotho levels with vascular pathology including vascular calcification and in vitro data of direct action of ?Klotho on both the endothelium and vascular smooth muscle cells in terms of cytoprotection and prevention of mineralization. Summary: It is critical to understand the pathogenic role of ?Klotho on the integral endothelium-vascular smooth muscle network rather than each cell type in isolation in uremic vasculopathy, as ?Klotho can serve as a potential prognostic biomarker and a biological therapeutic agent.
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Curr+Opin+Nephrol+Hypertens 2014 ; 23 (4): 331-9
