ArticleScientific reports2022
PFKM inhibits doxorubicin-induced cardiotoxicity by enhancing oxidative phosphorylation and glycolysis.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- PFKM acts as a metabolic switch initiating donut-shaped mitochondrial remodeling to promote osteogenesis.International journal of oral science · 2026Article
- Qishen Yiqi Dripping Pills ameliorate doxorubicin-induced cardiotoxicity: a study based on bioinformatics and experimental verification.Investigational new drugs · 2026Article
- Ethyl acetylsalicylate (E-ASA) protects against myocardial ischemia-reperfusion injury.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Transcriptomics and single-cell RNA sequencing uncover prognostic characteristics and immune regulatory mechanisms of lactylation in cervical cancer.BioImpacts : BI · 2026Article
- Proteomic analysis of Burkitt lymphoma tissues: insights into the impact of age and EBV infection on protein expression and molecular characteristics.Discover oncology · 2025Article
- A genome-wide association study identified 10 novel genomic loci associated with intrinsic capacity.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- ARRDC4-mediated glycolysis enhances innate immunity to influenza A virus through fructose-1,6-bisphosphate.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- PFKM Promotes the Progression of Gastric Cancer by Up-regulating CNTN1 Expression Through H3K18la Modification.Applied biochemistry and biotechnology · 2025Article
- Fenofibrate Differently Affects the Heart's Morphology and Metabolism in Young and Old Rats.International journal of molecular sciences · 2025Article
- Neuraminidase 1 Exacerbated Glycolytic Dysregulation and Cardiotoxicity by Destabilizing SIRT1 through Interactions with NRF2 and HIF1α.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transcriptomic Analysis of Muscle Satellite Cell Regulation on Intramuscular Preadipocyte Differentiation in Tan Sheep.International journal of molecular sciences · 2025Article
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- X-Chromosome-Linked miRNAs Regulate Sex Differences in Cardiac Physiology.Circulation research · 2025Article
- Status of Mitochondrial Oxidative Phosphorylation during the Development of Heart Failure.Antioxidants (Basel, Switzerland) · 2023Review
- Peptidase Inhibitor 16 Attenuates Left Ventricular Injury and Remodeling After Myocardial Infarction by Inhibiting the HDAC1-Wnt3a-β-Catenin Signaling Axis.Journal of the American Heart Association · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart failure (HF) is a global pandemic which affects about 26 million people. PFKM (Phosphofructokinase, Muscle), catalyzing the phosphorylation of fructose-6-phosphate, plays a very important role in cardiovascular diseases. However, the effect of PFKM in glycolysis and HF remains to be elucidated. H9c2 rat cardiomyocyte cells were treated with doxorubicin (DOX) to establish injury models, and the cell viability, apoptosis and glycolysis were measured. Quantitative reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting were used for gene expression. DOX treatment significantly inhibited PFKM expression in H9c2 cells. Overexpression of PFKM inhibited DOX-induced cell apoptosis and DOX-decreased glycolysis and oxidative phosphorylation (OXPHOS), while silencing PFKM promoted cell apoptosis and inhibited glycolysis and OXPHOS in H9c2 cells. Moreover, PFKM regulated DOX-mediated cell viability and apoptosis through glycolysis pathway. Mechanism study showed that histone deacetylase 1 (HDAC1) inhibited H3K27ac-induced transcription of PFKM in DOX-treated cells and regulated glycolysis. PFKM could inhibit DOX-induced cardiotoxicity by enhancing OXPHOS and glycolysis, which might benefit us in developing novel therapeutics for prevention or treatment of HF.
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