ArticleMolecular and cellular biochemistry2023
METTL3-modified lncRNA-SNHG8 binds to PTBP1 to regulate ALAS2 expression to increase oxidative stress and promote myocardial infarction.
Article in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- 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
- Interleukin enhancer binding factor 3 exacerbates cardiac inflammation and injury following myocardial infarction by inhibiting Lys48-linked ubiquitination on HNRNPA2B1 in macrophages.Cellular & molecular immunology · 2026Article
- PU.1 aggravates hepatic sinusoidal obstruction syndrome by upregulating PTBP1 and activating the Wnt/β-catenin pathway.Histology and histopathology · 2026Article
- The mechanism of m6A modification in cardiovascular diseases: A systematic review.Genes & diseases · 2026Review
- m6A modification on ncRNAs and underlying mechanisms of exercise in the regulation of pathological cardiac remodeling.European journal of medical research · 2025Review
- A review: oxidative stress in skeletal muscle and the non-coding RNAs behind it.Molecular and cellular biochemistry · 2025Review
- METTL3-Driven m6A Epigenetic Remodeling of lncRNA-AU020206 Stabilizes SLC7A11 via YTHDC2 Attenuates Apoptosis and Ferroptosis in Cerebral Ischemia/Reperfusion Injury.Biomolecules · 2025Article
- ZC3H13-Mediated m6A Modification Ameliorates Acute Myocardial Infarction through Preventing Inflammation, Oxidative Stress and Ferroptosis by Targeting lncRNA93358.Inflammation · 2025Article
- Orphan Nuclear Receptors TR2 and TR4 in Erythropoiesis: From Mechanisms to Therapies.Biomolecules · 2025Review
- Biological function of RNA-binding proteins in myocardial infarction: a potential emerging therapeutic limelight.Cell & bioscience · 2025Review
- METTL3-mediated m⁶A methylation in cardiac diseases: pathogenic roles and therapeutic potential.Cell biology and toxicology · 2025Review
- Emerging Roles of Long Non-Coding RNAs in Cardiovascular Diseases.Journal of cellular and molecular medicine · 2025Review
- Non-coding RNAs in heart failure: epigenetic regulatory mechanisms and therapeutic potential.Frontiers in genetics · 2025Review
- miRNAs Influence m6A RNA Methylation through FTO and IGF2BP2 in Pressure Overload-Induced Heart Failure.Combinatorial chemistry & high throughput screening · 2025Article
- Exercise Mediates Noncoding RNAs in Cardiovascular Diseases: Pathophysiological Roles and Clinical Application.Expert reviews in molecular medicine · 2024Review
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- WTAP-mediated mJournal of translational medicine · 2024Article
- N6-Methyladenosine Demethylase ALKBH5 Promotes Pyroptosis by Modulating PTBP1 mRNA Stability in LPS-Induced Myocardial Dysfunction.Acta Cardiologica Sinica · 2024Article
- m6A epitranscriptomic and epigenetic crosstalk in cardiac fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Review
- Regulatory mechanisms of long non-coding RNAs on mitochondrial function in congestive heart failure.Non-coding RNA research · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) is one of the important factors leading to death in today's society. Therefore, to study the related mechanism of MI and reduce myocardial ischemia-reperfusion injury is an important link to reduce MI injury. MI mice in vivo and cell model in vitro were constructed. The cardiac function and MI area of mice were detected, and myocardial tissue injury was detected by HE staining. ALAS2 expression in mice myocardial tissue was detected by IHC. The expressions of lncRNA-SNHG8, METTL3, PTBP1 and ALAS2 in myocardial tissue or cardiomyocytes were detected by qRT-PCR assay. MTT assay was used to measured viability of cardiomyocytes. The oxidative stress level in myocardial tissue or cardiomyocytes was detected by ELISA assay and ROS assay. RIP-qPCR and RNA pulldown assays determined the interaction between METTL3 and lncRNA-SNHG8, as well as PTBP1 and ALAS2. lncRNA-SNHG8 knockdown in MI mice was reduced myocardial infarction size, alleviated myocardial tissue injury and oxidative stress, and inhibited ALAS2 expression in myocardial tissue. RNA pulldown and RIP assays showed that lncRNA-SNHG8 binged with PTBP1 and PTBP1 interacted with ALAS2 mRNA. Knockdown of lncRNA-SNHG8, METTL3 or PTBP1 in MI cells enhanced viability of myocardial cells, attenuated ROS release and MDA level, increased SOD level, alleviated oxidative stress. ALAS overexpression attenuated the corresponding effect of knockdown of lncRNA-SNHG8 and/or PTBP1 on MI cells. In sum, our paper is demonstrated for the first time that METTL3 can promote lncRNA-SNHG8 through m6A modification, thereby regulating ALAS2 to induce oxidative stress and aggravate myocardial injury.
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Registered trials
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