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低氧诱导因子 1α 在脑缺血中的作用(综述)。

HIF‑1α in cerebral ischemia (Review).

机构信息

Institute of Traditional Chinese Medicine, Heilongjiang University of Traditional Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.

College of Pharmacy, Heilongjiang University of Traditional Chinese Medicine, Harbin, Heilongjiang 150040, P.R. China.

出版信息

Mol Med Rep. 2022 Feb;25(2). doi: 10.3892/mmr.2021.12557. Epub 2021 Dec 8.

DOI:10.3892/mmr.2021.12557
PMID:34878158
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8674706/
Abstract

Cerebral ischemic injury may lead to a series of serious brain diseases, death or different degrees of disability. Hypoxia‑inducible factor‑1α (HIF‑1α) is an oxygen‑sensitive transcription factor, which mediates the adaptive metabolic response to hypoxia and serves a key role in cerebral ischemia. HIF‑1α is the main molecule that responds to hypoxia. HIF‑1α serves an important role in the development of cerebral ischemia by participating in numerous processes, including metabolism, proliferation and angiogenesis. The present review focuses on the endogenous protective mechanism of cerebral ischemia and elaborates on the role of HIF‑1α in cerebral ischemia. In addition, it focuses on cerebral ischemia interventions that act on the HIF‑1α target, including biological factors, non‑coding RNA, hypoxic‑ischemic preconditioning and drugs, and expands upon the measures to strengthen the endogenous compensatory response to support HIF‑1α as a therapeutic target, thus providing novel suggestions for the treatment of cerebral ischemia.

摘要

脑缺血性损伤可能导致一系列严重的脑部疾病、死亡或不同程度的残疾。缺氧诱导因子-1α(HIF-1α)是一种氧敏感转录因子,介导对缺氧的适应性代谢反应,在脑缺血中起关键作用。HIF-1α 是对缺氧反应的主要分子。HIF-1α 通过参与包括代谢、增殖和血管生成在内的许多过程,在脑缺血的发展中发挥重要作用。本综述重点关注脑缺血的内源性保护机制,并详细阐述了 HIF-1α 在脑缺血中的作用。此外,还重点介绍了针对 HIF-1α 靶点的脑缺血干预措施,包括生物因子、非编码 RNA、缺氧缺血预处理和药物,并扩展了增强内源性代偿反应以支持 HIF-1α 作为治疗靶点的措施,从而为脑缺血的治疗提供新的建议。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/af45a23ef9d4/mmr-25-02-12557-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/b38d360a8dd9/mmr-25-02-12557-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/31910d7849a6/mmr-25-02-12557-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/af45a23ef9d4/mmr-25-02-12557-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/b38d360a8dd9/mmr-25-02-12557-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/31910d7849a6/mmr-25-02-12557-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/de4a/8674706/af45a23ef9d4/mmr-25-02-12557-g02.jpg

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