脑缺血中的缺氧诱导因子-1α通路:从分子机制到治疗靶点。

Veerta Sharma, Thakur Gurjeet Singh
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引用次数: 0

摘要

导言:脑缺血损伤可导致多种危及生命的情况、死亡或不同程度的残疾。缺氧诱导因子 1α(HIF 1α)是一种对氧敏感的转录因子,可控制对缺氧的适应性代谢反应,是脑缺血的重要组成部分。它参与代谢、增殖和血管生成等多个过程,在脑缺血中发挥着重要作用:方法:通过使用 Scopus、PubMed、Bentham 和 Elsevier 数据库等多个不同的搜索引擎,进行文献综述,以研究治疗脑缺血的 HIF-1α 通路的药理调节:结果:各种信号通路,如丝裂原活化蛋白激酶(MAPK)、Janus 激酶/信号转导和激活因子(JAK/STAT)、磷脂酰肌醇-3-激酶(PI3-K)和 cAMP 反应元件结合蛋白(CREB)在调节 HIF-1α 通路中发挥着重要作用,有助于预防脑缺血的发病机制:结论:通过各种分子信号通路(如 PI3-K、MAPK、CREB 和 JAK/STAT 激活剂)对 HIF-1α 通路进行药理调节,为未来干预和治疗脑缺血提供了广阔的前景。
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Hypoxia-inducible Factor-1α Pathway in Cerebral Ischemia: From Molecular Mechanisms to Therapeutic Targets.

Introduction: Ischemic injury to the brain can result in a variety of life-threatening conditions, mortality, or varying degrees of disability. Hypoxia-inducible factor 1α (HIF 1α), an oxygen- sensitive transcription factor that controls the adaptive metabolic response to hypoxia, is a critical constituent of cerebral ischemia. It participates in numerous processes, such as metabolism, proliferation, and angiogenesis, and plays a major role in cerebral ischemia.

Methods: Through the use of a number of different search engines like Scopus, PubMed, Bentham, and Elsevier databases, a literature review was carried out for investigating the pharmacological modulation of HIF-1α pathways for the treatment of cerebral ischemia.

Results: Various signalling pathways, such as Mitogen-activated protein kinase (MAPK), Janus kinase/ signal transducers and activators (JAK/STAT), Phosphoinositide-3-kinase (PI3-K), and cAMPresponse element binding protein (CREB) play a vital role in modulation of HIF-1α pathway, which helps in preventing the pathogenesis of cerebral ischemia.

Conclusion: The pharmacological modulation of the HIF-1α pathway via various molecular signalling pathways, such as PI3-K, MAPK, CREB, and JAK/STAT activators, offer a promising prospect for future interventions and treatment for cerebral ischemia.

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