线粒体动力学是细胞损伤和炎症反应的病理生理学的核心。在实体器官移植的背景下,线粒体与脑死亡后供体器官的免疫激活有关,因为它们对细胞应激反应的调节至关重要,细胞死亡,并通过根据细胞环境调整呼吸能力来显示能量适应性。线粒体损伤激活线粒体系统的裂变,聚变,生物发生,线粒体自噬,或线粒体自噬。已经研究了针对线粒体生理学的机制途径和疗法,作为减轻脑死亡对供体器官的负面影响的合理方法。尽管没有对整个领域的多重努力进行总结性评估。这篇小型评论旨在讨论供体脑死亡的相互作用,线粒体动力学,以及对同种异体移植功能的影响,肺,肝脏,和肾移植。
Mitochondrial dynamics are central to the pathophysiology of cellular damage and inflammatory responses. In the context of solid organ transplantation, mitochondria are implicated in immune activation in donor organs that occurs after brain death, as they are critical to the regulation of cellular stress response, cell death, and display energetic adaptations through the adjustment of respiratory capacity depending on the cellular milieu. Mitochondrial damage activates mitochondrial systems of fission, fusion, biogenesis, and mitochondrial autophagy, or mitophagy. The mechanistic pathways as well as therapies targeting mitochondrial physiology have been studied as plausible ways to mitigate the negative effects of brain death on donor organs, though there is no summative evaluation of the multiple efforts across the field. This mini-review aims to discuss the interplay of donor brain death, mitochondrial dynamics, and impact on allograft function as it pertains to heart, lung, liver, and kidney transplants.