ArticleExperimental & molecular medicine2017
miR-24-mediated knockdown of H2AX damages mitochondria and the insulin signaling pathway.
Article in Experimental & molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
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- Mitochondria-associated non-coding RNAs and their impact on drug resistance.Frontiers in pharmacology · 2025Review
- Investigation of the Presence of Papillomavirus in Bovine Testicles and Determination of γH2AX and Cytochrome C in Testicular Tissues Determined to be Infected.Veterinary medicine and science · 2025Article
- Lovastatin-Induced Mitochondrial Oxidative Stress Leads to the Release of mtDNA to Promote Apoptosis by Activating cGAS-STING Pathway in Human Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Synergistic effect of cold gas plasma and experimental drug exposure exhibits skin cancer toxicity in vitro and in vivo.Journal of advanced research · 2024Article
- Role of microRNAs in regulation of insulin secretion and insulin signaling involved in type 2 diabetes mellitus.Journal of biosciences · 2022Review
- MitomiRs: their roles in mitochondria and importance in cancer cell metabolism.Radiology and oncology · 2021Review
- Effect of Cold Atmospheric Plasma on Epigenetic Changes, DNA Damage, and Possibilities for Its Use in Synergistic Cancer Therapy.International journal of molecular sciences · 2021Review
- The genome variation and developmental transcriptome maps reveal genetic differentiation of skeletal muscle in pigs.PLoS genetics · 2021Article
- Mitochondrial microRNA (MitomiRs) in cancer and complex mitochondrial diseases: current status and future perspectives.Cellular and molecular life sciences : CMLS · 2021Review
- H2A.X Phosphorylation in Oxidative Stress and Risk Assessment in Plasma Medicine.Oxidative medicine and cellular longevity · 2021Review
- The lncRNA B3GALT5-AS1 Functions as an HCC Suppressor by Regulating the miR-934/UFM1 Axis.Journal of oncology · 2021Article
- Two genomes, one cell: Mitochondrial-nuclear coordination via epigenetic pathways.Molecular metabolism · 2020Review
- Elevated H2AX Phosphorylation Observed with kINPen Plasma Treatment Is Not Caused by ROS-Mediated DNA Damage but Is the Consequence of Apoptosis.Oxidative medicine and cellular longevity · 2019Article
- Long noncoding RNA B3GALT5-AS1 suppresses colon cancer liver metastasis via repressing microRNA-203.Aging · 2018Article
- Triple herbal extract DA-9805 exerts a neuroprotective effect via amelioration of mitochondrial damage in experimental models of Parkinson's disease.Scientific reports · 2018Article
- An in silico argument for mitochondrial microRNA as a determinant of primary non function in liver transplantation.Scientific reports · 2018Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial deficits or altered expressions of microRNAs are associated with the pathogenesis of various diseases, and microRNA-operated control of mitochondrial activity has been reported. Using a retrovirus-mediated short-hairpin RNA (shRNA) system, we observed that miR-24-mediated H2AX knockdown (H2AX-KD) impaired both mitochondria and the insulin signaling pathway. The overexpression of miR-24 decreased mitochondrial H2AX and disrupted mitochondrial function, as indicated by the ATP content, membrane potential and oxygen consumption. Similar mitochondrial damage was observed in shH2AX-mediated specific H2AX-KD cells. The H2AX-KD reduced the expression levels of mitochondrial transcription factor A (TFAM) and mitochondrial DNA-dependent transcripts. H2AX-KD mitochondria were swollen, and their cristae were destroyed. H2AX-KD also blocked the import of precursor proteins into mitochondria and the insulin-stimulated phosphorylation of IRS-1 (Y632) and Akt (S473 and T308). The rescue of H2AX, but not the nuclear form of ΔC24-H2AX, restored all features of miR-24- or shH2AX-mediated impairment of mitochondria. Hepatic miR-24 levels were significantly increased in db/db and ob/ob mice. A strong feedback loop may be present among miR-24, H2AX, mitochondria and the insulin signaling pathway. Our findings suggest that H2AX-targeting miR-24 may be a novel negative regulator of mitochondrial function and is implicated in the pathogenesis of insulin resistance.
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