TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated vascular smooth muscle cells.
TRPV1 activation impedes foam cell formation by inducing autophagy in oxLDL-treated vascular smooth muscle cells.
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TRPV1 激活通过诱导 oxLDL 处理的血管平滑肌细胞自噬来阻止泡沫细胞形成
DOI：
10.1038/cddis.2014.146
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发表时间：
2014-04-17
影响因子：
9
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中科院分区：
文献类型：
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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 泡沫细胞形成的机制相对鲜为人知。瞬时受体电位香草酸亚家族 1 (TRPV1) 和自噬的激活在调节泡沫细胞形成中具有潜在作用。我们的研究表明，在氧化低密度脂蛋白（oxLDL）处理的 VSMC 中，自噬可以防止泡沫细胞的形成。辣椒素激活 TRPV1 可挽救 oxLDL 损伤的自噬，并激活 VSMC 中的自噬-溶酶体途径；辣椒素激活 TRPV1，通过自噬诱导阻碍 VSMC 泡沫细胞的形成；辣椒素通过 AMP 激活蛋白激酶 (AMPK) 信号通路激活 TRPV1 诱导自噬。这项研究提供了证据，证明自噬在 VSMC 泡沫细胞形成中发挥重要作用，并强调 TRPV1 作为动脉粥样硬化的一个有前途的治疗靶点。
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.