Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095, USA.
Department of Integrative Biology and Physiology, University of California, Los Angeles, CA 90095, USA; Department of Neurosurgery, UCLA Brain Injury Research Center, University of California, Los Angeles, CA 90095, USA.
Pharmacol Res. 2024 Oct;208:107389. doi: 10.1016/j.phrs.2024.107389. Epub 2024 Sep 5.
Mitochondria provide the energy to keep cells alive and functioning and they have the capacity to influence highly complex molecular events. Mitochondria are essential to maintain cellular energy homeostasis that determines the course of neurological disorders, including traumatic brain injury (TBI). Various aspects of mitochondria metabolism such as autophagy can have long-term consequences for brain function and plasticity. In turn, mitochondria bioenergetics can impinge on molecular events associated with epigenetic modifications of DNA, which can extend cellular memory for a long time. Mitochondrial dysfunction leads to pathological manifestations such as oxidative stress, inflammation, and calcium imbalance that threaten brain plasticity and function. Hence, targeting mitochondrial function may have great potential to lessen the outcomes of TBI.
线粒体为细胞的存活和正常功能提供能量，并且具有影响高度复杂分子事件的能力。线粒体对于维持细胞能量稳态至关重要，而细胞能量稳态决定了包括创伤性脑损伤（TBI）在内的神经紊乱的进程。线粒体代谢的各个方面，如自噬，都可能对大脑功能和可塑性产生长期影响。反过来，线粒体生物能学又会影响与 DNA 表观遗传修饰相关的分子事件，从而延长细胞记忆。线粒体功能障碍会导致氧化应激、炎症和钙失衡等病理表现，威胁大脑的可塑性和功能。因此，靶向线粒体功能可能具有减轻 TBI 后果的巨大潜力。
