ArticleAmerican journal of translational research2022
Upregulation of SPI1 during myocardial infarction aggravates cardiac tissue injury and disease progression through activation of the TLR4/NFκB axis.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Multi-ancestry genetic architecture of heart failure subtypes.Nature communications · 2026Pooled it
- Identification of PANoptosis-related hub genes in acute myocardial infarction: diagnostic potential, immune correlates, and therapeutic insights.Journal of cardiothoracic surgery · 2026Article
- LncRNA FTX promotes myocardial fibrosis by sponging miR-335-3p to regulate TFEC/ILK signaling.Scientific reports · 2026Article
- hsa_circ_0004771-Targeted Adsorption of miR-429 Mediates ATP2A2 Expression to Attenuate Endoplasmic Reticulum Stress and Mitochondrial Dysfunction During Myocardial Infarction.Applied biochemistry and biotechnology · 2025Article
- Identification of biomarkers associated with phagocytosis regulatory factors in coronary artery disease using machine learning and network analysis.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- Computational analysis of congenital heart disease associated SNPs: unveiling their impact on the gene regulatory system.BMC genomics · 2025Article
- Identification and functional characterisation of DNA methylation differences between East- and West-originating Finns.Epigenetics · 2024Article
- Long non-coding RNA LncTUG1 regulates favourable compression force-induced cementocytes mineralization via PU.1/TLR4/SphK1 signalling.Cell proliferation · 2024Article
- A review on regulation of DNA methylation during post-myocardial infarction.Frontiers in pharmacology · 2024Review
- Effects of cage vs. net-floor mixed rearing system on goose spleen histomorphology and gene expression profiles.Frontiers in veterinary science · 2024Article
- Common ground on immune infiltration landscape and diagnostic biomarkers in diabetes-complicated atherosclerosis: an integrated bioinformatics analysis.Frontiers in endocrinology · 2024Article
- ATF3/SPI1/SLC31A1 Signaling Promotes Cuproptosis Induced by Advanced Glycosylation End Products in Diabetic Myocardial Injury.International journal of molecular sciences · 2023Article
- From multi-omics approaches to personalized medicine in myocardial infarction.Frontiers in cardiovascular medicine · 2023Review
- Article
- Identification of Hub Genes in the Remodeling of Non-Infarcted Myocardium Following Acute Myocardial Infarction.Journal of cardiovascular development and disease · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveSpleen focus forming virus proviral integration oncogene (SPI1) belongs to the ETS family of transcription factors participating in an array of cellular processes such as inflammation and cell apoptosis. This research focused on the role of SPI1 in the myocardial infarction (MI).
methodsA murine model of MI was established. HL-1 cells were exposed to hypoxic treatment to simulate an MI-like condition. Tissue injury, inflammatory infiltration, and fibrosis in the cardiac tissues, and the apoptosis and the production of inflammation-related factors in cells were examined. Expression of SPI1 was determined. The downstream targets of SPI1 were identified by bioinformatics tools and luciferase assays. Artificial up- or downregulation of SPI1 and toll like receptor 4 (TLR4) were induced to examine their involvements in MI progression.
resultsSPI1 was expressed at high levels in the cardiac tissues of MI mice and in hypoxia-induced HL-1 cells. SPI1 downregulation reduced apoptosis and the production of inflammatory cytokines in the hypoxia-induced HL-1 cells. SPI1 bound to TLR4 promoter to induce transcriptional activation. TLR4 induced NFκB phosphorylation and blocked the protective role of SPI1 silencing in cells.
conclusionThis study demonstrated that upregulation of SPI1, caused by reduced DNA methylation, augmented development of myocardial infarction by activating the TLR4/NFκB axis.
Indexed as
Identifiers
35559389PMC9091125W4285740842What OpenQuestion holds
Registered trials
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.