ArticleCirculation2019
Lin28a Regulates Pathological Cardiac Hypertrophic Growth Through Pck2-Mediated Enhancement of Anabolic Synthesis.
Article in Circulation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 46 citations in OpenAlex.
- From RCT to mechanistic study: ATRA reverses myofibroblast activation by reprogramming glucose metabolism via HIC1 and PCK1/2 to attenuate hypertrophic scar formation.Military Medical Research · 2026Trial
- Cardiac fibroblast deletion of PTBP1 modulates the profibrotic response by alternative splicing.Nature communications · 2026Article
- Inhibition of RBM25 preserves cardiac mitochondrial homeostasis and attenuates ischemic heart failure.Journal of molecular histology · 2026Article
- Non-telomeric function deficiency of TERT enhances pressure overload-induced mouse cardiac remodeling by activation of CNBP-mediated THBS3/ITGB1 pathway.Acta pharmacologica Sinica · 2026Article
- Protective role of HOXB5-orchestrated mitochondrial homeostasis and mitophagy in cardiomyocytes after ischemia-reperfusion via transcriptionally activating Sirt5.Cardiovascular drugs and therapy · 2026Article
- YY1/Asprosin/PFKP axis regulates glycolytic metabolic and exacerbates pathological cardiac hypertrophy.Nature communications · 2026Article
- Positron emission tomography reveals increased myocardial glucose uptake in a subset of Friedreich ataxia patients.Scientific reports · 2025Article
- A BACH1 inhibitor ameliorates myocardial infarction and limb ischemia in mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
- GSTM1 suppresses cardiac fibrosis post-myocardial infarction through inhibiting lipid peroxidation and ferroptosis.Military Medical Research · 2025Article
- Valerenic acid attenuates pathological myocardial hypertrophy by promoting the utilization of multiple substrates in the mitochondrial energy metabolism.Journal of advanced research · 2025Article
- Epigenetic Regulation of Cardiomyocyte Maturation by Arginine Methyltransferase CARM1.Circulation · 2024Article
- RNA-Binding Proteins in Cardiomyopathies.Journal of cardiovascular development and disease · 2024Review
- Analysis of immunoinfiltration and EndoMT based on TGF-β signaling pathway-related genes in acute myocardial infarction.Scientific reports · 2024Article
- Single-cell chromatin profiling reveals genetic programs activating proregenerative states in nonmyocyte cells.Science advances · 2024Article
- Advances in Metabolic Remodeling and Intervention Strategies in Heart Failure.Journal of cardiovascular translational research · 2024Review
- Metabolic adaptations in pressure overload hypertrophic heart.Heart failure reviews · 2024Review
- Activation of the integrated stress response rewires cardiac metabolism in Barth syndrome.Basic research in cardiology · 2023Article
- RNA-Binding Proteins as Critical Post-Transcriptional Regulators of Cardiac Regeneration.International journal of molecular sciences · 2023Review
- Dynamic interplay between RPL3- and RPL3L-containing ribosomes modulates mitochondrial activity in the mammalian heart.Nucleic acids research · 2023Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundHypertrophic response to pathological stimuli is a complex biological process that involves transcriptional and epigenetic regulation of the cardiac transcriptome. Although previous studies have implicated transcriptional factors and signaling molecules in pathological hypertrophy, the role of RNA-binding protein in this process has received little attention.
methodsHere we used transverse aortic constriction and in vitro cardiac hypertrophy models to characterize the role of an evolutionary conserved RNA-binding protein Lin28a in pathological cardiac hypertrophy. Next-generation sequencing, RNA immunoprecipitation, and gene expression analyses were applied to identify the downstream targets of Lin28a. Epistatic analysis, metabolic assays, and flux analysis were further used to characterize the effects of Lin28a and its downstream mediator in cardiomyocyte hypertrophic growth and metabolic remodeling.
resultsCardiac-specific deletion of Lin28a attenuated pressure overload-induced hypertrophic growth, cardiac dysfunction, and alterations in cardiac transcriptome. Mechanistically, Lin28a directly bound to mitochondrial phosphoenolpyruvate carboxykinase 2 ( Pck2) mRNA and increased its transcript level. Increasing Pck2 was sufficient to promote hypertrophic growth similar to that caused by increasing Lin28a, whereas knocking down Pck2 attenuated norepinephrine-induced cardiac hypertrophy. Epistatic analysis demonstrated that Pck2 mediated, at least in part, the role of Lin28a in cardiac hypertrophic growth. Furthermore, metabolomic analyses highlighted the role for Lin28a and Pck2 in promoting cardiac biosynthesis required for cell growth.
conclusionsOur study demonstrates that Lin28a promotes pathological cardiac hypertrophy and glycolytic reprograming, at least in part, by binding to and stabilizing Pck2 mRNA.
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