ArticleAging2022
piRNA-6426 increases DNMT3B-mediated SOAT1 methylation and improves heart failure.
Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Effects of exercise on peripheral blood DNA methylation and related epigenetic markers: a systematic review of human trials.Clinical epigenetics · 2026Pooled it
- The emerging roles of small nucleolar RNAs, piwi-interacting RNAs, tRNA-derived small RNAs, and circular RNAs in the regulation of cardiac hypertrophy, ischemic heart disease, and heart failure.Genes & diseases · 2026Review
- Nuclear m6A Methylase METTL3 Drives Production of ITGβ4E to Exacerbate Heart Failure via SRSF3-Mediated Alternative Splicing of ITGβ4.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- PIWI-Interacting RNAs in Cardiovascular Disease: From Epigenetic Regulators to Clinical Biomarkers and Therapeutic Targets.Reviews in cardiovascular medicine · 2026Review
- Review
- Integration of short non coding RNA and genetic factors for coronary artery disease risk prediction in a prospective study.Scientific reports · 2026Article
- Cardiomyocyte programmed cell death in dilated cardiomyopathy: molecular crosstalk and therapeutic implications.Frontiers in cell and developmental biology · 2026Review
- DNA Methylation Patterns of 5mC Regulators: Insights into Immune Microenvironment Regulation in Heart Failure.Applied biochemistry and biotechnology · 2026Article
- N4-acetylcytidine-mediated SOAT1 upregulation aggravates heart failure by inducing NCOA4-dependent ferroautophagy and ferroptosis in cardiomyocytes.Cellular and molecular life sciences : CMLS · 2025Article
- The PIWI-interacting RNA CRAPIR alleviates myocardial ischemia‒reperfusion injury by reducing p53-mediated apoptosis via binding to SRSF1.Acta pharmacologica Sinica · 2025Article
- The significance of small noncoding RNAs in the pathogenesis of cardiovascular diseases.Genes & diseases · 2025Review
- piENOX2 regulates ALKBH5-mediated Itga4 mExperimental & molecular medicine · 2025Article
- piRNAs as Potential Regulators of Mammary Gland Development and Pathology in Livestock.Veterinary sciences · 2025Review
- Regulatory roles of PIWI-interacting RNAs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2025Review
- Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.Nature reviews. Cardiology · 2024Review
- The potential emerging role of piRNA/PIWI complex in virus infection.Virus genes · 2024Review
- Recent advances of PIWI-interacting RNA in cardiovascular diseases.Clinical and translational medicine · 2024Review
- Potential molecular mechanisms and clinical implications of piRNAs in preeclampsia: a review.Reproductive biology and endocrinology : RB&E · 2024Review
- Comprehensive prognostic and immune analysis of sterol O-acyltransferase 1 in patients with hepatocellular carcinoma.World journal of hepatology · 2024Article
- Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePrevious studies found that piRNAs could participate in disease progression by regulating DNA methylation, but there are few reports on their roles in heart failure (HF).
methodsThe level of piRNA-6426 in the venous blood of HF patients and volunteers was detected by RT-qPCR. Hypoxia-induced cardiomyocytes were transfected with lentiviral-mediated piRNA-6426 overexpression vector (LV-piRNA-6426) or together with LV-DNMT3B, and then cell viability and apoptosis, glucose uptake, ROS production, LDH activity and secretion of inflammatory factors were detected. Also, cardiomyocytes were transfected with LV-piRNA-6426, sh-piRNA-6426 or sh-SOAT1, as well as LV-piRNA-6426 or together with LV-DNMT3B or sh-DNMT3B. The interaction between piRNA-6426 and methyltransferase 3B (DNMT3B) was detected with RNA immunoprecipitation (RIP). And the methylation level of sterol o-acyltransferase 1 (SOAT1) and the enrichment of DNMT3B in the SOAT1 promoter were detected with Methylation-specific PCR (MSP) and ChIP assays. Then a HF rat model constructed with coronary artery occlusion method was injected with LV-piRNA-6426, and heart function index and infarcted area of rat heart were detected.
resultspiRNA-6426 expression was decreased in the blood of HF patients. LV-piRNA-6426 transfection increased the enrichment of DNMT3B in SOAT1 promoter, thereby inhibiting the expression level of SOAT1, and decreased hypoxia-induced oxidative stress and inflammation in cardiomyocytes, while sh-piRNA-6426 transfection had the opposite effect. And LV-DNMT3B transfection enhanced the effect of LV-piRNA-6426 transfection on SOAT1 expression and cardiomyocyte dysfunction. Injection of LV-piRNA-6426 significantly inhibited the heart dysfunction of rats.
conclusionspiRNA-6426 overexpression inhibits hypoxia-induced cardiomyocyte dysfunction and HF by promoting DNMT3B-mediated methylation of SOAT1 promoter.
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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.