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2000
Volume 24, Issue 3
  • ISSN: 1871-5273
  • E-ISSN: 1996-3181

Abstract

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 cAMP-response 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 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.

© 2024 Bentham Science Publishers
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/content/journals/cnsnddt/10.2174/0118715273324551241008111827
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Hypoxia-inducible Factor-1α Pathway in Cerebral Ischemia: From Molecular Mechanisms to Therapeutic Targets
CNS & Neurological Disorders - Drug Targets (Formerly Current Drug Targets - CNS & Neurological Disorders) 24, 208 (2025); https://doi.org/10.2174/0118715273324551241008111827
/content/journals/cnsnddt/10.2174/0118715273324551241008111827
/content/journals/cnsnddt/10.2174/0118715273324551241008111827
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  • Article Type:     Review Article
Keyword(s): angiogenesis; cerebral ischemia; hypoxia response elements; Hypoxia-inducible factor-1α; ischemic stroke; neuroinflammation; neurotransmitters

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