ArticleNature metabolism2020
Mitochondrial pyruvate carrier abundance mediates pathological cardiac hypertrophy.
Article in Nature metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
82 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- A narrative review of metabolomics approaches in identifying biomarkers of doxorubicin-induced cardiotoxicity.Metabolomics : Official journal of the Metabolomic Society · 2025Pooled it
- Lactylation at the metabolic-epigenetic interface in cardiovascular diseases: context-dependent mechanisms and translational roadmap.Journal of advanced research · 2026Review
- The functional role of the circular RNA circCDR1as targeting SERCA2a in the progression of pathological cardiac hypertrophy and heart failure.Journal of translational medicine · 2026Article
- Sam68 Exacerbates Pathologic Cardiac Hypertrophy by Suppressing Cardiomyocyte Glucose Oxidation.Circulation · 2026Article
- [3-Npj imaging · 2026Article
- Defects in auxiliary fuel oxidation and mitochondrial pyruvate transport mark transition to overt heart failure in Tgαq*44 mice.Journal of translational medicine · 2026Article
- Fumarate hydratase ameliorates pressure overload induced cardiac remodeling by controlling Elovl7-mediated biosynthesis of unsaturated fatty acids.Acta pharmacologica Sinica · 2026Article
- Metabolic reprogramming in diabetes and other endocrine and metabolic disorders: exploring the Warburg effect, ketones, and SGLT2 inhibitors.Reviews in endocrine & metabolic disorders · 2026Review
- Article
- HuoXue QianYang QuTan recipe attenuates myocardial hypertrophy in obese hypertensive rats by regulating MPC1/MCT4 mediated pyruvate-lactate metabolic axis.Chinese medicine · 2025Article
- Review
- The crosstalk between immune activation and metabolism in heart failure. A scientific statement of the Heart Failure Association of the ESC.European journal of heart failure · 2025Review
- The fate of pyruvate dictates cell growth by modulating cellular redox potential.bioRxiv : the preprint server for biology · 2025Article
- Peptide Drug: Design and Clinical Applications.MedComm · 2025Review
- Oral Sulforaphane Intervention Protects Against Diabetic Cardiomyopathy in db/db Mice: Focus on Cardiac Lipotoxicity and Substrate Metabolism.Antioxidants (Basel, Switzerland) · 2025Article
- Article
- Loss of mitochondrial pyruvate transport initiates cardiac glycogen accumulation and heart failure.bioRxiv : the preprint server for biology · 2025Article
- Article
- Leptin drives glucose metabolism to promote cardiac protection via OPA1-mediated HDAC5 translocation and Glut4 transcription.Functional & integrative genomics · 2025Article
- Energy metabolism in cardiovascular diseases: unlocking the hidden powerhouse of cardiac pathophysiology.Frontiers in endocrinology · 2025Review
22 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 3 countries.
Funding
Abstract
Cardiomyocytes rely on metabolic substrates, not only to fuel cardiac output, but also for growth and remodelling during stress. Here we show that mitochondrial pyruvate carrier (MPC) abundance mediates pathological cardiac hypertrophy. MPC abundance was reduced in failing hypertrophic human hearts, as well as in the myocardium of mice induced to fail by angiotensin II or through transverse aortic constriction. Constitutive knockout of cardiomyocyte MPC1/2 in mice resulted in cardiac hypertrophy and reduced survival, while tamoxifen-induced cardiomyocyte-specific reduction of MPC1/2 to the attenuated levels observed during pressure overload was sufficient to induce hypertrophy with impaired cardiac function. Failing hearts from cardiomyocyte-restricted knockout mice displayed increased abundance of anabolic metabolites, including amino acids and pentose phosphate pathway intermediates and reducing cofactors. These hearts showed a concomitant decrease in carbon flux into mitochondrial tricarboxylic acid cycle intermediates, as corroborated by complementary 1,2-[
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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.