肝脏缺血再灌注损伤中的代谢重编程：线粒体、脂质代谢与铁死亡之间的交互对话
Metabolic reprogramming in hepatic ischemia-reperfusion injury: crosstalk between mitochondria, lipid metabolism, and ferroptosis.
摘要(中文译文)
肝脏缺血再灌注损伤是肝脏手术、移植和创伤中临床上重要的并发症，涉及氧化应激、炎症、免疫信号传导、微循环功能障碍、代谢紊乱和调节性细胞死亡。本综述并不旨在对所有肝脏缺血再灌注损伤机制进行全面概述，而是聚焦于代谢重编程作为连接线粒体功能障碍、脂质代谢重塑和铁死亡的整合性框架。在缺血期间，缺氧和三磷酸腺苷耗竭可能抑制CPT1A相关的脂肪酸氧化，促进脂质蓄积和代谢应激。在再灌注期间，线粒体活性氧生成、钙调节异常和线粒体质量控制失衡可能与磷脂重塑相互作用，增加脂质过氧化的易感性。铁死亡被讨论为一种调节性过程，其驱动因素不仅包括铁过载，还包括GPX4依赖性脂质过氧化物解毒功能受损以及Nrf2/SLC7A11/HO-1轴等抗氧化通路的失调。本综述的核心信息是，肝脏缺血再灌注损伤的进展可能反映的是一个依赖具体情境的线粒体-脂质代谢-铁死亡网络，而非孤立的或线性的损伤通路。这一框架可能有助于识别共享的治疗节点，同时认识到若干机制仍具有模型依赖性，需要进一步验证。
Abstract
Hepatic ischemia-reperfusion injury is a clinically important complication of liver surgery, transplantation, and trauma, involving oxidative stress, inflammation, immune signaling, microcirculatory dysfunction, metabolic disturbance, and regulated cell death. This review does not aim to provide an exhaustive overview of all hepatic ischemia-reperfusion injury mechanisms, but instead focuses on metabolic reprogramming as an integrative framework linking mitochondrial dysfunction, lipid metabolic remodeling, and ferroptosis. During ischemia, oxygen deprivation and adenosine triphosphate depletion may suppress CPT1A-related fatty acid oxidation, promoting lipid accumulation and metabolic stress. During reperfusion, mitochondrial reactive oxygen species generation, Ca dysregulation, and mitochondrial quality-control imbalance may interact with phospholipid remodeling to increase lipid peroxidation susceptibility. Ferroptosis is discussed as a regulated process driven not only by iron overload, but also by impaired GPX4-dependent lipid peroxide detoxification and dysregulated antioxidant pathways such as the Nrf2/SLC7A11/HO-1 axis. The key message of this review is that hepatic ischemia-reperfusion injury progression may reflect a context-dependent mitochondria-lipid metabolism-ferroptosis network rather than isolated or linear injury pathways. This framework may help identify shared therapeutic nodes while recognizing that several mechanisms remain model-dependent and require further validation.
如何引用
AMA
Jiebin Pan, Junhao Feng, Zixuan Ding, Mengru Fang, Wenxin Yu, Lu Yang, et al. Metabolic reprogramming in hepatic ischemia-reperfusion injury: crosstalk between mitochondria, lipid metabolism, and ferroptosis.. Biochemical and biophysical research communications. 2026; doi:10.1016/j.bbrc.2026.154044.
APA
Jiebin Pan, Junhao Feng, Zixuan Ding, Mengru Fang, Wenxin Yu, Lu Yang, et al (2026). Metabolic reprogramming in hepatic ischemia-reperfusion injury: crosstalk between mitochondria, lipid metabolism, and ferroptosis.. Biochemical and biophysical research communications. https://doi.org/10.1016/j.bbrc.2026.154044
GB/T 7714
Jiebin Pan, Junhao Feng, Zixuan Ding, Mengru Fang, Wenxin Yu, Lu Yang, et al. Metabolic reprogramming in hepatic ischemia-reperfusion injury: crosstalk between mitochondria, lipid metabolism, and ferroptosis.[J]. Biochemical and biophysical research communications, 2026 doi:10.1016/j.bbrc.2026.154044.
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