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Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shandong Medical Journal is the property of Shandong Medical Health Newspapers and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

脑缺血后再灌注可引发多种分子级联反应，加重神经元损伤，导致受损线粒体堆积，造成脑缺血再灌注损 伤（CIRI）。线粒体功能障碍可诱导线粒体自噬，通过消除受损或去极化线粒体来维持细胞稳态，在 CIRI的病理过 程中至关重要。在CIRI中，多种信号通路和线粒体自噬受体蛋白通过介导线粒体自噬发挥重要作用，包括MAPK/ ERK/CREB 通路、PI3K/Akt/mTOR 通路、PINK1/Parkin/p62 通路，以及 BNIP3/Nix、FUNDC1、LC3/p62、VDAC1、 Beclin-1、Drp1、Opa1等蛋白。调控线粒体相关的自噬信号通路及关键蛋白可能成为保护神经细胞、治疗CIRI的关 键靶点，对治疗CIRI具有重要意义。 [ABSTRACT FROM AUTHOR]

心肌缺血再灌注时,心肌线粒体的结构和功能受到多种因素的影响导致线粒体功能障碍,可引起线粒体ATP生成减少、Ca2+超载、活性氧暴涨、线粒体跨膜电位降低以及膜通透性提高,这些因素最终会导致线粒体过度自噬以及内源性细胞凋亡和坏死,心肌细胞死亡数目急剧上升,出现心肌缺血再灌注损伤(MIRI)。通过对MIRI患者线粒体功能障碍的靶向治疗,给予尼克地尔、雷帕霉素等靶向药物,抑制线粒体功能障碍引起的不良事件,可减轻线粒体损伤,从而改善心肌细胞活力和减轻MIRI。 [ABSTRACT FROM AUTHOR]

Copyright of Journal of Kunming Medical University / Kunming Yike Daxue Xuebao is the property of Kunming Medical Journal and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

线粒体脂肪酸氧化异常、呼吸链受损、能量代谢障碍均可导致线粒体功能障碍，从而使 ＡＴＰ 合成减少， ＲＯＳ的消耗量减少但含量仍在增加；而过量的 ＲＯＳ 又能再次引起氧化应激反应和脂质过氧化反应，进而加重线粒 体损伤，引起肝脏脂质沉积，从而加剧肝脏的氧化应激反应，导致肝细胞凋亡。氧化应激和肝细胞凋亡是非酒精性 脂肪肝（ＮＡＦＬＤ）发生、进展的核心环节。氧化应激可导致炎性因子释放增多、多种促凋亡因子表达增强、加剧肝细 胞线粒体能量代谢障碍，导致肝细胞发生炎症、凋亡或坏死，使病程向脂肪性肝炎及肝纤维化发展。线粒体功能的改变往往先于临床症状出现，及时察觉其功能的改变并做相应的处理，可阻止或延缓疾病的进一步发生、发展. [ABSTRACT FROM AUTHOR]