Hunan Provincial Key Laboratory for Special Pathogens Prevention and Control, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Institute of Pathogenic Biology, Hengyang Medical School, University of South China, Hengyang, China.
Front Cell Infect Microbiol. 2022 Mar 7;12:835181. doi: 10.3389/fcimb.2022.835181. eCollection 2022.
Mitochondria are intracellular organelles that are instrumental in the creation of energy, metabolism, apoptosis, and intrinsic immunity. Mitochondria exhibit an extraordinarily high degree of flexibility, and are constantly undergoing dynamic fusion and fission changes. is an intracellular bacterium that causes serious health problems in both humans and animals. Due to a deficiency of multiple metabolic enzymes, these pathogenic bacteria are highly dependent on their eukaryotic host cells, resulting in a close link between infection and host cell mitochondria. Indeed, increase mitochondrial fusion by inhibiting the activation of dynein-related protein 1 (DRP1), which can regulate host cell metabolism for extra energy. Additionally, can inhibit mitochondrial fission by blocking DRP1 oligomerization, preventing host cell apoptosis. These mechanisms are critical for maintaining a favorable environment for reproduction and growth of . This review discusses the molecular mechanisms of mitochondrial fusion and fission, as well as the mechanisms by which infection alters the mitochondrial dynamics and the prospects of limiting chlamydial development by altering mitochondrial dynamics.
线粒体是细胞内的细胞器，在能量产生、代谢、细胞凋亡和固有免疫中起着重要作用。线粒体具有极高的灵活性，不断进行动态融合和裂变变化。 是一种细胞内细菌，可导致人类和动物严重的健康问题。由于缺乏多种代谢酶，这些病原菌高度依赖其真核宿主细胞，导致 感染与宿主细胞线粒体之间存在密切联系。事实上， 通过抑制动力蛋白相关蛋白 1（DRP1）的激活来增加线粒体融合，从而可以调节宿主细胞代谢以获取额外的能量。此外， 通过阻止 DRP1 寡聚化来抑制线粒体裂变，从而阻止宿主细胞凋亡。这些机制对于维持 的繁殖和生长的有利环境至关重要。本综述讨论了线粒体融合和裂变的分子机制，以及 感染如何改变线粒体动力学的机制，以及通过改变线粒体动力学来限制衣原体发育的前景。
