Evidence map›Paper›PMID 40735300›Full record

ArticleIBRO neuroscience reports2025

Beclin1-mediated vascular autophagy negatively regulates angiogenesis and secondary neural damage in the thalamus following cerebral cortical infarction.

Mengzhi Liu, Yuqian Chen, Xinyan Fan, Jinmin Gu, Shihui Xing

Abstract read
In one paragraph

Article in IBRO neuroscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Mengzhi LiuDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Yuqian ChenDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Xinyan FanDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Jinmin GuDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Shihui XingDepartment of Neurology and Stroke Center, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Focal cerebral infarction induces angiogenesis in the thalamus, which influences cognitive recovery. However, the mechanisms of angiogenesis in the thalamus remain unclear. This study was designed to investigate the potential role of Beclin1-mediated vascular autophagy in angiogenesis occurring in the thalamus after cerebral infarction. Cerebral infarction was induced by middle cerebral artery occlusion (MCAO). Cognitive function was evaluated using the Morris Water Maze. We assessed secondary neuronal damage, angiogenesis, Beclin1 expression and vascular autophagy in blood vessels of the ipsilateral thalamus. The functional effects of Beclin1 on vascular autophagy, angiogenesis and angiogenesis-related factors were determined using lentiviral-delivered siRNA. The results revealed significant angiogenesis in the ipsilateral thalamus at 7 days after MCAO, concurrent with elevated LC3-I to LC3-II conversion and increased Beclin1 expression in the ipsilateral thalamic vessels. Knockdown of Beclin1 markedly suppressed vascular autophagic activation and potentiated thalamic angiogenesis at the above time point. This enhanced angiogenesis correlated with significant reductions of neuronal loss and astrogliosis in the ipsilateral thalamus, alongside improved cognitive function. Furthermore, Beclin1 knockdown significantly increased the levels of angiopoietin-2 (ANG-2) and vascular endothelial growth factor (VEGF) in the ipsilateral thalamus after cerebral infarction. Collectively, these findings implicate that inhibition of Beclin1-mediated vascular autophagy enhances angiogenesis and mitigates secondary thalamic neuronal damage following cerebral infarction. This neuroprotective effect likely related to the restoration of ANG-2 and VEGF levels mediated by vascular autophagy in the thalamus.

Indexed as

AngiogenesisAutophagyBeclin1Cerebral infarctionThalamus

Identifiers

PMID40735300
PMCPMC12304704

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