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TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated vascular smooth muscle cells

机译:TRPV1激活通过在oxLDL处理的血管平滑肌细胞中诱导自噬来阻止泡沫细胞形成

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Vascular smooth muscle cells (VSMCs) are an important origin of foam cells besides macrophages. The mechanisms underlying VSMC foam cell formation are relatively little known. Activation of transient receptor potential vanilloid subfamily 1 (TRPV1) and autophagy have a potential role in regulating foam cell formation. Our study demonstrated that autophagy protected against foam cell formation in oxidized low-density lipoprotein (oxLDL)-treated VSMCs; activation of TRPV1 by capsaicin rescued the autophagy impaired by oxLDL and activated autophagy–lysosome pathway in VSMCs; activation of TRPV1 by capsaicin impeded foam cell formation of VSMCs through autophagy induction; activation of TRPV1 by capsaicin induced autophagy through AMP-activated protein kinase (AMPK) signaling pathway. This study provides evidence that autophagy plays an important role in VSMC foam cell formation and highlights TRPV1 as a promising therapeutic target in atherosclerosis.
机译:除巨噬细胞外,血管平滑肌细胞(VSMC)是泡沫细胞的重要来源。 VSMC泡沫泡孔形成的机理还鲜为人知。瞬时受体电位香草样亚家族1(TRPV1)的激活和自噬在调节泡沫细胞形成中具有潜在作用。我们的研究表明,自噬可防止氧化低密度脂蛋白(oxLDL)处理的VSMC中形成泡沫细胞。辣椒素激活TRPV1可以挽救oxLDL损伤的自噬,并激活VSMC中的自噬-溶酶体途径。辣椒素对TRPV1的激活阻碍了自噬诱导VSMCs泡沫细胞的形成;辣椒素通过AMP激活的蛋白激酶(AMPK)信号传导途径诱导TRPV1的自噬。这项研究提供的证据表明自噬在VSMC泡沫细胞形成中起着重要作用,并突出了TRPV1作为动脉粥样硬化的有希望的治疗靶点。

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