Celastrol ameliorates vascular neointimal hyperplasia through Wnt5a-involved autophagy.
Celastrol ameliorates vascular neointimal hyperplasia through Wnt5a-involved autophagy.
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雷公藤红醇通过 Wnt5a 相关的自噬改善血管新生内膜增生
DOI：
10.7150/ijbs.58715
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发表时间：
2021
影响因子：
9.2
通讯作者：
Qin L
中科院分区：
文献类型：
--
作者：
Shi YN;Liu LP;Deng CF;Zhao TJ;Shi Z;Yan JY;Gong YZ;Liao DF;Qin L
血管平滑肌细胞（VSMCs）过度增生引起的内膜增生是再狭窄的病理基础。然而，很少有有效的策略来防止再狭窄。Celastrol，一种五环三萜，最近被证明对某些心血管疾病有益。基于其对细胞自噬的显著影响，我们提出雷公藤红素可能通过增强VSMCs的自噬来减轻再狭窄。本研究发现，雷公藤红素通过诱导细胞自噬，有效抑制VSMCs的内膜增生和过度增生。结果表明，雷公藤红素促进细胞自噬可诱导c-MYC溶酶体降解，这可能是抑制VSMCs增殖的机制之一。发现Wnt5a/PKC/mTOR信号通路是雷公酚诱导自噬和抑制VSMCs增殖的潜在机制。这些观察结果表明，celastrol可能是一种具有很大潜力的预防再狭窄的新药。
Neointimal hyperplasia caused by the excessive proliferation of vascular smooth muscle cells (VSMCs) is the pathological basis of restenosis. However, there are few effective strategies to prevent restenosis. Celastrol, a pentacyclic triterpene, has been recently documented to be beneficial to certain cardiovascular diseases. Based on its significant effect on autophagy, we proposed that celastrol could attenuate restenosis through enhancing autophagy of VSMCs. In the present study, we found that celastrol effectively inhibited the intimal hyperplasia and hyperproliferation of VSMCs by inducing autophagy. It was revealed that autophagy promoted by celastrol could induce the lysosomal degradation of c-MYC, which might be a possible mechanism contributing to the reduction of VSMCs proliferation. The Wnt5a/PKC/mTOR signaling pathway was found to be an underlying mechanism for celastrol to induce autophagy and inhibit the VSMCs proliferation. These observations indicate that celastrol may be a novel drug with a great potential to prevent restenosis.
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