血红素氧合酶-1/一氧化碳系统对脓毒症肺损伤时细胞器调控作用的研究进展
Research advances of the regulation of heme oxygenase-1/carbon monoxide system on organelles during sepsis-induced acute lung injury
摘要脓毒症急性肺损伤(acute lung injury, ALI)发病急骤,是临床常见的急危重症。研究表明,线粒体动力学、内质网应激(endoplasmic reticulum stress, ERs)、高尔基体应激、溶酶体介导细胞自噬、外泌体分泌转移等细胞器功能障碍在脓毒症ALI发生发展的病理生理过程中发挥重要作用。血红素氧合酶-1(heme oxygenase-1, HO-1)及其催化产物一氧化碳(carbon monoxide,CO)是应激状态下细胞重要的内源性保护机制之一,通过发挥抗氧化应激、抗炎、抗凋亡等作用以减轻脓毒症ALI。文章主要阐述HO-1/CO系统对脓毒症ALI时细胞内各重要细胞器如线粒体、内质网、高尔基体、溶酶体、外泌体等的调控作用,为脓毒症ALI基于发病机制的治疗提供新途径和理论依据。
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abstractsSepsis-induced acute lung injury (ALI) is a rapid onset, typical clinical intensive emergency. Studies have shown that mitochondrial dynamics, endoplasmic reticulum stress (ERs), Golgi apparatus stress, lysosome-mediated autophagy, exosome secretion and transfer play an essential role in the pathophysiological process of septic ALI. Heme oxygenase-1 (HO-1) and its catalytic byproducts, carbon monoxide (CO), are one of the crucial endogenous protective mechanisms of cells under stress, which can alleviate septic ALI through antioxidant, anti-inflammatory, and anti-apoptosis effects. This review mainly elaborates the role of HO-1/CO system in regulating the intracellular key organelles such as mitochondria, endoplasmic reticulum, golgi apparatus, lysosome, exosome in the settings of septic ALI, which provides a new approach and theoretical basis for the prevention and treatment of septic ALI.
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