Evidence map›Paper›PMID 41004172›Full record

ArticleBioscience reports2025

High expression of Fgr in the left ventricle attenuates myocardial injury in the infarcted region via regulating the phosphorylation level of PI3K/Akt.

Dongpu Shao, Zhiguo Zhang, Honglei Ji, Lei Shi

Abstract read
In one paragraph

Article in Bioscience reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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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

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3 · Its place in the literature

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4 · The record

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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

4 authors.

Dongpu ShaoDepartment of Cardiology, First Hospital of Jilin University, Changchun, Jilin, 130021, China.ORCID 0009-0001-7216-9353
Zhiguo ZhangDepartment of Cardiology, First Hospital of Jilin University, Changchun, Jilin, 130021, China.ORCID 0000-0002-4501-6423
Honglei Ji *Department of Cardiology, First Hospital of Jilin University, Changchun, Jilin, 130021, China.ORCID 0009-0009-9053-5220
Lei Shi *Department of Cardiology, First Hospital of Jilin University, Changchun, Jilin, 130021, China.ORCID 0009-0005-9862-9580

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FGR proto-oncogene (Fgr), a member of the Src family kinases, has garnered attention for its potential involvement in apoptotic signaling, yet its role in cardiovascular diseases, particularly acute myocardial infarction (AMI), remains unexplored. This study sought to investigate whether elevated left ventricular Fgr expression alleviates myocardial injury in the infarcted area and whether this protective mechanism is mediated by modulating phosphoinositide 3-kinase (PI3K)/Akt phosphorylation. The transcriptome-wide association study was initially utilized to screen for susceptibility genes in the left ventricle, with findings validated using bulk-RNA sequencing data from a rat model of left anterior descending coronary artery (LAD) ligation; subsequently, human spatial transcriptomics combined with single-nucleus RNA sequencing data confirmed differential expression of Fgr and PI3K/Akt in the infarcted region. Fgr knockdown via siRNA in H9C2 cells and pharmacological inhibition with TL02-59 in rats were conducted to assess cellular survival and cardiac function, respectively. Fgr emerged as a common candidate gene identified through multi-omics data analysis, with its up-regulation confirmed both in vivo and in vitro. Fgr silencing in an in vitro oxygenglucose deprivation model significantly reduced cell survival and suppressed PI3K/Akt phosphorylation, whereas TL02-59 administration in rats subjected to LAD ligation impaired post-infarction cardiac function while concurrently inhibiting PI3K/Akt phosphorylation levels. This study demonstrates that Fgr is markedly up-regulated in AMI and exerts cardioprotective effects, possibly through modulation of PI3K/Akt signaling phosphorylation, thereby underscoring its potential as a therapeutic target.

Indexed as

Heart VentriclesMyocardial InfarctionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktsrc-Family KinasesAnimalsCell LineDisease Models, AnimalHumansMaleMyocytes, CardiacPhosphorylationProto-Oncogene MasRatsRats, Sprague-DawleySignal TransductionMAS1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene MasProto-Oncogene Proteins c-aktsrc-Family KinasesFgrmyocardial infarctionPI3K/AktSingle-nucleus RNA sequencingspatial transcriptomicsTWAS

Identifiers

PMID41004172
PMCPMC12784349

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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.