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Effects of Mitochondrial Potassium Channel and Membrane Potential on Hypoxic Human Pulmonary Artery Smooth Muscle Cells

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收录情况： ◇ SCIE

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单位： [1]Fudan Univ, Zhongshan Hosp, Dept Resp Med, Shanghai 200433, Peoples R China [2]Wenzhou Med Coll, Affiliated Hosp 1, Dept Resp Med, Wenzhou 325000, Peoples R China [3]Huazhong Univ Sci & Technol, Tongji Hosp, Dept Resp Med, Wuhan 430074, Peoples R China

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关键词： pulmonary artery smooth muscle cells hypoxia mitochondrial K-ATP channels mitochondrial membrane potential cytochrome C apoptosis

摘要：

Chronic hypoxia induces proliferation of human pulmonary artery smooth muscle cells (hPASMCs), leading to remodeling and pulmonary hypertension, but the mechanism remains unclear. The present study tested the roles of mitochondrial ATP-sensitive potassium channel (mitoK(ATP)) and mitochondrial membrane potential (Delta Psi(m)) on hPASMCs under normoxic or hypoxic conditions. Our results demonstrated that diazoxide or hypoxia, alone or in combination, could depolarize Delta Psi(m) through opening mitoK(ATP), release of cytochrome C, and overproduction of hydrogen peroxide by mitochondria, resulting in increased proliferation and decreased apoptosis of hPASMCs. Five-hydroxydecanoate could partly reduce these hypoxia-dependent responses. These results suggest that the opening of mitoK(ATP) followed by a depolarization of Delta Psi(m) might play an important role in hypoxic proliferation of hPASMCs through cytochrome C accumulation within the mitochondria or mitochondrial overproduction of hydrogen peroxide.

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出版当年[2009]版：

大类 | 2 区生物

小类 | 2 区呼吸系统 3 区生化与分子生物学 3 区细胞生物学

最新[2025]版：

大类 | 2 区医学

小类 | 2 区生化与分子生物学 2 区细胞生物学 2 区呼吸系统

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出版当年[2008]版：

Q1 RESPIRATORY SYSTEM Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q2 CELL BIOLOGY

最新[2023]版：

Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY Q1 RESPIRATORY SYSTEM Q2 CELL BIOLOGY

影响因子： 5.9 最新[2023版] 6.2 最新五年平均 4.477 出版当年[2008版] 4.282 出版当年五年平均 4.608 出版前一年[2007版] 4.319 出版后一年[2009版]

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第一作者单位： [2]Wenzhou Med Coll, Affiliated Hosp 1, Dept Resp Med, Wenzhou 325000, Peoples R China

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