Visfatin from Adipocyte Accelerates Vascular Calcification via TLR4
Abstract
Abstract Background: Vascular calcification is a common complication in metabolic diseases, such as diabetes and obesity, contributing to cardiovascular morbidity. Visfatin, an adipokine secreted by visceral fat, has been confirmed to be closely associated with metabolic dysfunctions. Methods: Vascular calcification models were established in mice through intraperitoneal injection of vitamin D (VitD). Serum visfatin levels were measured in both patients with coronary artery calcification and calcified mice. Visfatin expression in visceral fat was assessed by molecular analyses. To examine the functional role of visfatin, mice with adipose-specific visfatin overexpression were generated. Primary vascular smooth muscle cells (VSMCs) were treated with calcification medium and recombinant visfatin to assess osteogenic differentiation. The interaction between visfatin and Toll-like receptor 4 (TLR4) was investigated, and Tlr4 knockout models were used to verify its role. Empagliflozin was administered to evaluate its effects on vascular calcification and visfatin expression, along with related signaling pathway analyses. Results: Serum visfatin levels were significantly elevated in patients with high coronary artery calcification scores and in mice with vascular calcification compared to controls. Visfatin expression was also markedly increased in the visceral adipose tissue of calcified mice. Mice with adipose-specific visfatin overexpression showed aggravated vascular…
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