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Updated: Mar 17, 2026

Vasodilation of Isolated Vessels and the Isolation of the Extracellular Matrix of Tight-skin Mice
Published on: March 24, 2017
Irisin reverses platelet derived growth factor-BB-induced vascular smooth muscle cells phenotype modulation through
Haibo Song1, Jia Xu2, Nan Lv3
1State Key Laboratory of Microbial Technology, School of Life Sciences, Shandong University, Jinan, 250100, China; Center for Gene and Immunotherapy, The Second Hospital of Shandong University, Jinan, 250012, China.
Abstract:
Vascular smooth muscle cells (VSMCs) phenotype modulation toward a synthetic phenotype is the main cause of cardiovascular disease. As a newly discovered myokine, Irisin is thought to be a promising candidate for the treatment of metabolic disturbances, as well as cardiovascular disease. However, no evidence has been shown for the direct effect of Irisin on VSMCs phenotype modulation and its underling mechanisms. The aim of this study was to explore the effect of Irisin on VSMCs phenotype modulation and the mechanisms involved. In the present study, it was found that Irisin restored the PDGF-BB-induced VSMCs phenotype modulation which exhibited down-regulation of smooth muscle cells (SMC) expression and up-regulation of matrix synthesis related marker expression, as well as proliferative phenotype. Moreover, our research demonstrated that Irisin further activated STAT3 signaling pathways. Finally, by applying an STAT3 inhibitor, WP1066, we revealed the roles of STAT3 in the PDGF-BB-induced VSMCs phenotype modulation when they were treated with Irisin. Taken together, these results demonstrated that Irisin may play a crucial role in regulating VSMCs phenotype modulation via the STAT3 signaling pathway.
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