Visfatin aggravates transverse aortic constriction‐induced cardiac remodelling by enhancing macrophage‐mediated oxidative stress in mice

Abstract

Previous studies have reported that visfatin can regulate macrophage polarisation, which has been demonstrated to participate in cardiac remodelling. The aims of this study were to investigate whether visfatin participates in transverse aortic constriction (TAC)‐induced cardiac remodelling by regulating macrophage polarisation. First, TAC surgery and angiotensin II (Ang II) infusion were used to establish a mouse cardiac remodelling model, visfatin expression was measured, and the results showed that TAC surgery or Ang II infusion increased visfatin expression in the serum and heart in mice, and phenylephrine or hydrogen peroxide promoted the release of visfatin from macrophages in vitro. All these effects were dose‐dependently reduced by superoxide dismutase. Second, visfatin was administered to TAC mice to observe the effects of visfatin on cardiac remodelling. We found that visfatin increased the cross‐sectional area of cardiomyocytes, aggravated cardiac fibrosis, exacerbated cardiac dysfunction, further regulated macrophage polarisation and aggravated oxidative stress in TAC mice. Finally, macrophages were depleted in TAC mice to investigate whether macrophages mediate the regulatory effect of visfatin on cardiac remodelling, and the results showed that the aggravating effects of visfatin on oxidative stress and cardiac remodelling were abrogated. Our study suggests that visfatin enhances cardiac remodelling by promoting macrophage polarisation and enhancing oxidative stress. Visfatin may be a potential target for the prevention and treatment of clinical cardiac remodelling.

Chinese visceral adipose index is more closely associated with risk of arterial stiffness than traditional obesity indicators: a cohort study

“…Visfatin increased oxidative stress [43], the production of matrix metalloproteinases (such as MMP-9) [44], and collagen deposition. Adiponectin was one of the few anti-in ammatory and protective adipokines.…”

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“…Серцеві ефекти вісфатину. Вісфатин сприяє карді-альному фіброзу, стимулюючи проліферацію кардіальних фібробластів у щурів та активуючи дозрівання проколагену І та ІІІ в цих клітинах [21,42]. Зростання рівня циркуляторного вісфатину корелює зі ступенем нестабільності атеросклеротичних бляшок та оклюзії артерії в зоні некротичного ураження міокарда (infarct-related artery).…”

Macrophage Polarization in Left Ventricular Structural Remodeling Induced by Hypertension

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