Study summary · research use only
IGF-1 has plaque-stabilizing effects in atherosclerosis by altering vascular smooth muscle cell phenotype
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study combined in vitro experiments on murine vascular smooth muscle cells (vSMCs) with in vivo experiments in apolipoprotein E knockout mice to examine IGF-1 signaling and plaque phenotype in atherosclerosis. M1-polarized macrophage-conditioned medium was reported to inhibit IGF-1 signaling, increase vSMC apoptosis, decrease proliferation, and reduce α-actin and col3a1 expression while increasing matrix-degrading enzyme expression; these effects were reported as correctable by IGF-1 supplementation. In vivo, the stable IGF-1 analog Long R3 IGF-1 was associated with reduced stenosis and core size and a doubled cap/core ratio in early atherosclerosis, and in advanced plaques increased vSMC content more than twofold while reducing intraplaque hemorrhage rate. The authors interpreted these findings as consistent with a role for IGF-1 in plaque stability through effects on smooth muscle cell turnover and phenotype.
Abstract
Insulin-like growth factor-1 (IGF-1) signaling is important for the maintenance of plaque stability in atherosclerosis due to its effects on vascular smooth muscle cell (vSMC) phenotype. To investigate this hypothesis, we studied the effects of the highly inflammatory milieu of the atherosclerotic plaque on IGF-1 signaling and stability-related phenotypic parameters of murine vSMCs in vitro, and the effects of IGF-1 supplementation on plaque phenotype in an atherosclerotic mouse model. M1-polarized, macrophage-conditioned medium inhibited IGF-1 signaling by ablating IGF-1 and increasing IGF-binding protein 3, increased vSMC apoptosis, and decreased proliferation. Expression of α-actin and col3a1 genes was strongly attenuated by macrophage-conditioned medium, whereas expression of matrix-degrading enzymes was increased. Importantly, all of these effects could be corrected by supplementation with IGF-1. In vivo, treatment with the stable IGF-1 analog Long R3 IGF-1 in apolipoprotein E knockout mice reduced stenosis and core size, and doubled cap/core ratio in early atherosclerosis. In advanced plaques, Long R3 IGF-1 increased the vSMC content of the plaque by more than twofold and significantly reduced the rate of intraplaque hemorrhage. We believe that IGF-1 in atherosclerotic plaques may have a role in preventing plaque instability, not only by modulating smooth muscle cell turnover, but also by altering smooth muscle cell phenotype.
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