Evidence map›Paper›PMID 40261607›Full record

ArticleMolecular neurobiology2025

Silencing Hmox1 Attenuates Cerebral Ischemia/reperfusion Injury and Inhibits Inflammation and Ferroptosis Via the PPAR-γ/FABP4 Signaling Pathway.

Zhigang Li, Kai Huang, Jie Cao, Mingwei Guo, Haifa Dong, Weisheng Ye, Songbing Zeng, Jianing Wei, Qiujiang Xi

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In one paragraph

Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Identification of HMOX-1-Targeting Natural Compounds inPharmaceuticals (Basel, Switzerland) · 2025
    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.

Zhigang LiDepartment of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China.
Kai HuangSchool of the Frist Clinical Medicine, Gannan Medical University, Ganzhou City, China.
Jie CaoDepartment of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China.
Mingwei GuoDepartment of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China.
Haifa DongDepartment of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China.
Weisheng YeDepartment of Neurology, Longnan Hospital, the First Affiliated Hospital of Gannan Medical University, No. 128 Jinling Road, Zhanggong District, Ganzhou City, 341000, Jiangxi Province, China.
Songbing ZengSchool of the Frist Clinical Medicine, Gannan Medical University, Ganzhou City, China.
Jianing WeiSchool of the Frist Clinical Medicine, Gannan Medical University, Ganzhou City, China.
Qiujiang XiDepartment of Neurology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China. Xiqiujiang992437@sina.com.

Funding

Ganzhou Key Laboratory of Translational Medicine of Cerebrovascular Disease 20230101-35National Natural Science Foundation of China 81460187
6 · The paper itself

Abstract

Cerebral ischemia/reperfusion (I/R) may aggravate tissue injury by promoting oxidative stress, inflammation and cell death after ischemic injury. This study aimed to identify cerebral I/R-associated hub genes and to reveal the underlying mechanism on ischemic I/R. Differential expressed genes (DEGs) were identified from the Gene Expression Omnibus (GEO) database, and hub genes were screened from a protein-protein interaction (PPI) network. The I/R rat model was constructed using the middle cerebral artery occlusion and reperfusion (MCAO/R), and Hmox1 was silenced to investigate its effects on I/R injury, inflammation, oxidative stress and ferroptosis. The effects of silencing Hmox1 were also evaluated in OGD/R-treated HT22 cells. The inhibitor of peroxisome proliferator-activated receptor (PPAR)-γ pathway, T0070907, was used to determine the regulation of Hmox1 on the PPAR-γ/fatty acid binding protein 4 (FABP4) pathway. Heme oxygenase 1 (Hmox1), matrix metalloproteinase-13 (Mmp13), CD44 molecule (Cd44), C-C motif chemokine ligand 3 (Ccl3) and serpin family B member 5 (Serpinb5) were selected as hub genes with higher expression in MCAO/R rats. Silencing Hmox1 inhibited cell apoptosis, decreased tumor necrosis factor-α (TNF-α), Interleukin-1β (IL-1β), IL-6, Fe

Indexed as

Brain IschemiaFatty Acid-Binding ProteinsFerroptosisGene SilencingHeme Oxygenase-1InflammationPPAR gammaReperfusion InjurySignal TransductionAnimalsCell LineHeme Oxygenase (Decyclizing)Infarction, Middle Cerebral ArteryMaleMiceOxidative StressFatty Acid-Binding ProteinsHeme Oxygenase-1Heme Oxygenase (Decyclizing)Hmox1 protein, ratPPAR gammaDifferential expressed genesFerroptosisHeme oxygenase 1InflammationIschemia/reperfusion

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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.