当前位置: X-MOL 学术Cell Prolif. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
ERK/Drp1-dependent mitochondrial fission contributes to HMGB1-induced autophagy in pulmonary arterial hypertension
Cell Proliferation ( IF 8.5 ) Pub Date : 2021-05-04 , DOI: 10.1111/cpr.13048
Wei Feng 1 , Jian Wang 1 , Xin Yan 1 , Qianqian Zhang 1 , Limin Chai 1 , Qingting Wang 1 , Wenhua Shi 1 , Yuqian Chen 1 , Jin Liu 1 , Zhan Qu 1 , Shaojun Li 1 , Xinming Xie 1 , Manxiang Li 1
Affiliation  

High-mobility group box-1 (HMGB1) and aberrant mitochondrial fission mediated by excessive activation of GTPase dynamin-related protein 1 (Drp1) have been found to be elevated in patients with pulmonary arterial hypertension (PAH) and critically implicated in PAH pathogenesis. However, it remains unknown whether Drp1-mediated mitochondrial fission and which downstream targets of mitochondrial fission mediate HMGB1-induced pulmonary arterial smooth muscle cells (PASMCs) proliferation and migration leading to vascular remodelling in PAH. This study aims to address these issues.

中文翻译:

ERK/Drp1 依赖性线粒体裂变有助于 HMGB1 诱导的肺动脉高压自噬

已发现高迁移率族框 1 (HMGB1) 和由 GTPase 动力相关蛋白 1 (Drp1) 过度激活介导的异常线粒体裂变在肺动脉高压 (PAH) 患者中升高,并且与 PAH 发病机制密切相关。然而,Drp1 介导的线粒体裂变和线粒体裂变的下游靶点是否介导 HMGB1 诱导的肺动脉平滑肌细胞 (PASMCs) 增殖和迁移,导致 PAH 中的血管重塑,尚不清楚。本研究旨在解决这些问题。
更新日期:2021-06-01
down
wechat
bug