ArticleJournal of cellular and molecular medicine2021
PKM2 promotes angiotensin-II-induced cardiac remodelling by activating TGF-β/Smad2/3 and Jak2/Stat3 pathways through oxidative stress.
Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 54 citations in OpenAlex.
- Roles of inflammation and metabolic dysfunction in cardiovascular diseases: molecular mechanisms and therapeutic targets.Molecular biomedicine · 2026Review
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- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- METTL3 mediates mJournal of advanced research · 2026Article
- Qianyang Yuyin granule modulates glycolysis and inflammatory response to treat hypertensive cardiac remodeling.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026Article
- Metabolic reprogramming in cardiac fibrosis: mechanisms, crosstalk, and therapeutic interventions.Frontiers in physiology · 2026Review
- Amelioration of CKD-induced cardiomyocyte hypertrophy by pegmolesatide: involvement of JAK2/STAT3 inhibition and mitochondrial protection.Frontiers in pharmacology · 2026Article
- Identification of novel biomarkers for hypertension and ventricular remodeling based on transcriptomics and machine learning.iScience · 2025Article
- Review
- PFKFB3 Promotes Myofibroblast Differentiation and Cardiac Fibrosis Through its Intra- and Extra- Cellular Roles.Journal of cardiovascular translational research · 2025Article
- Beyond Thrombosis: Pulmonary Hypertension and Heart Failure in Patients With Myeloproliferative Neoplasms: JACC: CardioOncology State-of-the-Art Review.JACC. CardioOncology · 2025Review
- Increased Plasma Pyruvate Kinase M2 (PK-M2) in Heart Failure: A Novel Biomarker Related to Cardiac Function and its Clinical Implications.Journal of the American Heart Association · 2025Article
- Loss of PKM2 dysregulates inflammatory signaling in the infarcted murine heart.Physiological reports · 2025Article
- Cardiovascular Risk in Philadelphia-Negative Myeloproliferative Neoplasms: Mechanisms and Implications-A Narrative Review.Current issues in molecular biology · 2024Review
- Pyruvate kinase M2 sustains cardiac mitochondrial quality surveillance in septic cardiomyopathy by regulating prohibitin 2 abundance via S91 phosphorylation.Cellular and molecular life sciences : CMLS · 2024Article
- Search progress of pyruvate kinase M2 (PKM2) in organ fibrosis.Molecular biology reports · 2024Review
- TGF-β Isoforms and GDF-15 in the Development and Progression of Atherosclerosis.International journal of molecular sciences · 2024Review
- Shikonin alleviates doxorubicin-induced cardiotoxicity via Mst1/Nrf2 pathway in mice.Scientific reports · 2024Article
- PKM2 interacts with and phosphorylates PHB2 to sustain mitochondrial quality control against septic cerebral-cardiac injury.International journal of medical sciences · 2024Article
- Inhibition of Pyruvate kinase M2 (PKM2) by shikonin attenuates isoproterenol-induced acute myocardial infarction via reduction in inflammation, hypoxia, apoptosis, and fibrosis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hypertensive cardiac remodelling is a common cause of heart failure. However, the molecular mechanisms regulating cardiac remodelling remain unclear. Pyruvate kinase isozyme type M2 (PKM2) is a key regulator of the processes of glycolysis and oxidative phosphorylation, but the roles in cardiac remodelling remain unknown. In the present study, we found that PKM2 was enhanced in angiotensin II (Ang II)-treated cardiac fibroblasts and hypertensive mouse hearts. Suppression of PKM2 by shikonin alleviated cardiomyocyte hypertrophy and fibrosis in Ang-II-induced cardiac remodelling in vivo. Furthermore, inhibition of PKM2 markedly attenuated the function of cardiac fibroblasts including proliferation, migration and collagen synthesis in vitro. Mechanistically, suppression of PKM2 inhibited cardiac remodelling by suppressing TGF-β/Smad2/3, Jak2/Stat3 signalling pathways and oxidative stress. Together, this study suggests that PKM2 is an aggravator in Ang-II-mediated cardiac remodelling. The negative modulation of PKM2 may provide a promising therapeutic approach for hypertensive cardiac remodelling.
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