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Updated: Jul 26, 2025

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Hypoxic Postconditioning Promotes Angiogenesis After Ischemic Stroke.

Wenjie Shi1, Changhong Ren2, Wei Zhang3

  • 1North China University of Science and Technology Affiliated Hospital, Tangshan 063000, China; Beijing Key Laboratory of Hypoxia Translational Medicine, Xuanwu Hospital, Capital Medical University, Beijing 100053, China.

Neuroscience
|June 18, 2023
PubMed
Summary

Hypoxic postconditioning (HPC) promotes angiogenesis and improves neurological function after ischemic stroke. This protective effect may involve the PLCλ and ALK5 pathways, enhancing recovery from brain injury.

Keywords:
angiogenesishypoxic postconditioningischemic strokeneuroprotection

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Area of Science:

  • Neuroscience
  • Cardiovascular Biology
  • Cell Biology

Background:

  • Hypoxic postconditioning (HPC) offers neuroprotection in ischemic stroke, but its impact on post-stroke angiogenesis remains largely unknown.
  • Understanding HPC's role in angiogenesis is crucial for developing novel therapeutic strategies for stroke recovery.

Purpose of the Study:

  • To investigate the effects of HPC on angiogenesis following ischemic stroke.
  • To explore the underlying mechanisms, including the involvement of specific signaling pathways.

Main Methods:

  • In vitro: Oxygen-glucose deprivation (OGD) model using bEnd.3 cells to assess proliferation, migration, and tube formation.
  • In vivo: Middle cerebral artery occlusion (MCAO) model in mice to evaluate neurological deficits and angiogenesis via immunofluorescence and Western blot.

Main Results:

  • HPC significantly enhanced endothelial cell proliferation, migration, and tube formation in vitro.
  • HPC treatment improved neurological scores and promoted angiogenesis in the peri-infarct region of MCAO mice.
  • Angiogenesis levels correlated positively with neurological recovery, and HPC upregulated PLCλ and ALK5 expression.

Conclusions:

  • HPC ameliorates neurological deficits in focal cerebral ischemia by promoting angiogenesis.
  • The pro-angiogenic effects of HPC in stroke recovery may be mediated by the PLCλ and ALK5 signaling pathways.