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血管过氧化物(O_2~-)和炎症可导致高血压。线粒体是O_2~-的重要来源,然而,线粒体O_2~-的调控和将线粒体作为治疗靶点所体现出的潜在降压作用尚未明确。血管紧张素Ⅱ和炎性细胞因子,如白细胞介素17A和肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)可显著促进高血压的发生发展。研究人员假设血管紧张素Ⅱ和细胞因子协同作用,导致亲环蛋白D(cyclophilin D,CypD)依赖的线粒体O_2~-的生成,进
Vascular peroxides (O 2 -) and inflammation can lead to high blood pressure. Mitochondria are important sources of O 2 - -, however, the regulation of mitochondrial O 2 - and the potential antihypertensive effects of mitochondria as therapeutic targets are not yet clear. Angiotensin II and inflammatory cytokines such as interleukin 17A and tumor necrosis factor-α (TNF-α) can significantly promote the development of hypertension. The researchers hypothesized that the synergistic effect of angiotensin II and cytokines results in the generation of cyclophilin D (CypD) -dependent mitochondrial O 2 -