ArticleBiomedical journal2022
AIFM1, negatively regulated by miR-145-5p, aggravates hypoxia-induced cardiomyocyte injury.
Article in Biomedical journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- MiR-145-5p modulates collagen production and fibroblast behaviour after cardiac injury partially via COL5A1.Basic research in cardiology · 2026Article
- An Integrated Cardiac Microtissue Proteome Map Extends Therapeutic Remodeling by Nanovesicles.Molecular & cellular proteomics : MCP · 2026Article
- LncRNA OTUD6B-AS1 overexpression induces parthanatos in esophageal adenocarcinoma cells by binding to miR-145-5p and promoting AIF expression.American journal of translational research · 2026Article
- Integrative PANoptosis-focused omics analysis uncovers GSDMC as a candidate biomarker in breast cancer.Frontiers in cell and developmental biology · 2026Article
- circSP199a, a circularized RNA sponge targeting miR-199a-5p and -3p, mitigates mouse cardiac hypertrophy and fibrosis.Acta pharmacologica Sinica · 2026Article
- Intranasal delivery of hypoxia-preconditioned extracellular vesicles derived from BMSCs alleviates neuroinflammation and brain dysfunction in TBI.Stem cell research & therapy · 2025Article
- Uncovering the new landscape of leukoaraiosis through the circular RNA-miRNA-mRNA axis.Frontiers in neurology · 2025Article
- Innovative Therapeutic Strategies for Myocardial Infarction Across Various Stages: Non-Coding RNA and Stem Cells.International journal of molecular sciences · 2024Review
- The Mitochondrial Blueprint: Unlocking Secondary Metabolite Production.Metabolites · 2024Review
- Mechanism Actions of Coniferyl Alcohol in Improving Cardiac Dysfunction in Renovascular Hypertension Studied by Experimental Verification and Network Pharmacology.International journal of molecular sciences · 2024Article
- Unraveling the differential mechanisms of revascularization promoted by MSCs & ECFCs from adipose tissue or umbilical cord in a murine model of critical limb-threatening ischemia.Journal of biomedical science · 2024Article
- P-MSC-derived extracellular vesicles facilitate diabetic wound healing via miR-145-5p/ CDKN1A-mediated functional improvements of high glucose-induced senescent fibroblasts.Burns & trauma · 2023Article
- M2 macrophage-derived exosomal miR-145-5p protects against the hypoxia/reoxygenation-induced pyroptosis of cardiomyocytes by inhibiting TLR4 expression.Annals of translational medicine · 2022Article
- Small and mighty - microRNAs pulling the strings.Biomedical journal · 2022Article
- Unveiling Human Proteome Signatures of Heart Failure with Preserved Ejection Fraction.Biomedicines · 2022Article
- CircularRNA circ_0071269 knockdown protects against from diabetic cardiomyopathy injury by microRNA-145/gasdermin A axis.Bioengineered · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia-induced apoptosis is linked to the pathogenesis of myocardial infarction. The role of apoptosis-inducing factor mitochondria associated 1 (AIFM1) in cardiomyocyte injury remains unclear. This study was aimed at probing into the role and the underlying regulatory mechanism of AIFM1 in myocardial injury.
methodsH9c2 cardiomyocytes and C57BL/6 mice were used for myocardial hypoxic/ischemic injury and myocardial infarction animal models. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to evaluate the expression levels of AIFM1 mRNA and miR-145-5p. Western blot was used for examining the expression levels of AIFM1, caspase-3, cleaved caspase-3, p-53, and γ-H2AX. Cell viability was examined by cell counting kit-8 (CCK-8) assay and BrdU assay. Interaction between AIFM1 and miR-145-5p was determined by bioinformatics analysis, qRT-PCR, Western blot, and dual-luciferase reporter assay.
resultsAIFM1 expression was markedly highly elevated, while miR-145-5p expression was significantly down-regulated in the myocardial infarction animal model and H9c2 cells under hypoxia. Augmentation of AIFM1 led to a dramatic decrease of cell viability, accompanied by an increase of the secretion of the inflammatory cytokines IL-1β, TNF-α, IL-6, and the expression of cleaved caspase-3. Furthermore, AIFM1 was identified as a target of miR-145-5p. In addition, miR-145-5p/AIFM1 axis regulated the expression of p53.
conclusionAIFM1 may exacerbate myocardial ischemic injury by promoting inflammation and the injury of cardiomyocytes, and its up-regulation may be partly due to the down-regulation of miR-145-5p.
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