Evidence map›Paper›PMID 39072998›Full record

ArticleCNS neuroscience & therapeutics2024

The p75 neurotrophin receptor attenuates secondary thalamic damage after cortical infarction by promoting angiogenesis.

Linhui Peng, Kongping Li, Dan Li, Xialin Zuo, Lixuan Zhan, Meiyan Chen, Ming Gong, Weiwen Sun, En Xu

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. NF-Frontiers in cardiovascular medicine · 2026
    Article
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Linhui PengDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Kongping LiDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Dan LiDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Xialin ZuoDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Lixuan ZhanDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Meiyan ChenDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Ming GongDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
Weiwen SunDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.
En XuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, Guangdong, China.ORCID 0000-0003-4874-6373

Funding

National Natural Science Foundation of China 81971233Science and Technology Program of Guangzhou, China 2023A04J1203Science and Technology Program of Guangzhou, China 2024A03J0199
6 · The paper itself

Abstract

backgroundAngiogenesis is crucial in neuroprotection of secondary thalamic injury after cortical infarction. The p75 neurotrophin receptor (p75

methodsThe male rat model of dMCAO was established. The effects of p75

resultsWe found that the p75

conclusionFor the first time, we highlighted that the enhancement of p75

Indexed as

Infarction, Middle Cerebral ArteryNeovascularization, PhysiologicRats, Sprague-DawleyThalamusAngiogenesisAnimalsCerebral InfarctionHypoxia-Inducible Factor 1, alpha SubunitMaleNerve Tissue ProteinsRatsReceptors, Growth FactorReceptors, Nerve Growth FactorVascular Endothelial Growth Factor AHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitNerve Tissue ProteinsNgfr protein, ratReceptors, Growth FactorReceptors, Nerve Growth FactorVascular Endothelial Growth Factor Avascular endothelial growth factor A, ratangiogenesiscortical infarctionHIF‐1αp75NTRsecondary damagethalamus

Identifiers

PMID39072998
PMCPMC11284236

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.