AMPK: The key to ischemia-reperfusion injury

IF 4 2区 生物学 Q2 CELL BIOLOGY
Jie Cai, Xinyue Chen, Xingyu Liu, Zhangwang Li, Ao Shi, Xiaoyi Tang, Panpan Xia, Jing Zhang, Peng Yu
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引用次数: 12

Abstract

Ischemia-reperfusion injury (IRI) refers to a syndrome in which tissue damage is further aggravated and organ function further deteriorates when blood flow is restored after a period of tissue ischemia. Acute myocardial infarction, stress ulcer, pancreatitis, intestinal ischemia, intermittent claudication, acute tubular necrosis, postshock liver failure, and multisystem organ failure are all related to reperfusion injury. AMP-activated protein kinase (AMPK) has been identified in multiple catabolic and anabolic signaling pathways. The functions of AMPK during health and diseases are intriguing but still need further research. Except for its conventional roles as an intracellular energy switch, emerging evidence reveals the critical role of AMPK in IRI as an energy-sensing signal molecule by regulating metabolism, autophagy, oxidative stress, inflammation, and other progressions. At the same time, drugs based on AMPK for the treatment of IRI are constantly being researched and applied in clinics. In this review, we summarize the mechanisms underlying the effects of AMPK in IRI and describe the AMPK-targeting drugs in treatment, hoping to increase the understanding of AMPK in IRI and provide new insights into future clinical treatment.

AMPK:缺血再灌注损伤的关键
缺血再灌注损伤(ischemia -reperfusion injury, IRI)是指组织缺血一段时间后血流恢复,组织损伤进一步加重,器官功能进一步恶化的综合征。急性心肌梗死、应激性溃疡、胰腺炎、肠缺血、间歇性跛行、急性肾小管坏死、休克后肝衰竭、多系统脏器功能衰竭等均与再灌注损伤有关。amp活化蛋白激酶(AMPK)在多种分解代谢和合成代谢信号通路中被发现。AMPK在健康和疾病中的作用是有趣的,但仍需要进一步研究。除了其作为细胞内能量开关的传统作用外,越来越多的证据表明,AMPK作为一种能量传感信号分子,通过调节代谢、自噬、氧化应激、炎症和其他进展,在IRI中发挥着关键作用。同时,基于AMPK的治疗IRI的药物也在不断地被研究和应用于临床。本文综述了AMPK在IRI中的作用机制,并介绍了目前针对AMPK的治疗药物,希望能增加对AMPK在IRI中的认识,并为未来的临床治疗提供新的见解。
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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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