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http://purl.uniprot.org/citations/34863964http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/34863964http://www.w3.org/2000/01/rdf-schema#comment"

Background

Hypoxia-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.

Methods

H9c2 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.

Results

AIFM1 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.

Conclusion

AIFM1 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."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.org/dc/terms/identifier"doi:10.1016/j.bj.2021.11.012"xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Chen S."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Zhu H."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Zhou W."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Gao P."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Ruan C."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Ji L."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Shi N."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Tu D."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/author"Yangqu W."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/date"2022"xsd:gYear
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/name"Biomed J"xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/pages"870-882"xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/title"AIFM1, negatively regulated by miR-145-5p, aggravates hypoxia-induced cardiomyocyte injury."xsd:string
http://purl.uniprot.org/citations/34863964http://purl.uniprot.org/core/volume"45"xsd:string
http://purl.uniprot.org/citations/34863964http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/34863964
http://purl.uniprot.org/citations/34863964http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/34863964
http://purl.uniprot.org/uniprot/#_B1AU25-mappedCitation-34863964http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34863964
http://purl.uniprot.org/uniprot/#_Q9Z0X1-mappedCitation-34863964http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/34863964
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