Atherosclerosis constitutes a pathological process underlying cardiovascular diseases. There is growing evidence that
IGFBP5 is a causative factor, although the conclusions of different studies are inconsistent. The present study aims to confirm the role and mechanism of
IGFBP5 in atherosclerosis. The expression of
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Atherosclerosis constitutes a pathological process underlying cardiovascular diseases. There is growing evidence that
IGFBP5 is a causative factor, although the conclusions of different studies are inconsistent. The present study aims to confirm the role and mechanism of
IGFBP5 in atherosclerosis. The expression of
IGFBP5 was induced in the skeletal muscle of male ApoE
−/− mice, an atherosclerosis model, using adeno-associated virus, resulting in elevated circulating
IGFBP5 levels. Changes in blood lipids were detected, and pathological changes in the aorta were observed. Analysis of
IGFBP5 function using RNA sequencing and validation were performed in a mouse aortic smooth muscle cell line. The results demonstrated that
IGFBP5 overexpression exacerbated the development of aortic lesions in this murine models without any discernible alterations in lipid profile parameters; the arterial transcriptomic landscape revealed that heightened
IGFBP5 levels predominantly influenced pathways governing smooth muscle cell proliferation and motility. In vitro experimentation corroborated these findings, showcasing the stimulatory effect of
IGFBP5 on VSMC (vascular smooth muscle cell) proliferation and migration, provoking a transition toward a proliferative phenotype.
IGFBP5 promotes atherosclerosis in ApoE
−/− mice through the phenotypic transformation of VSMCs. This finding suggests that
IGFBP5 has the potential to serve as an indicator of atherosclerosis diagnosis and a target for therapeutic interventions in the future.
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