ArticleCardiovascular drugs and therapy2021
Matrix Metalloproteinases Repress Hypertrophic Growth in Cardiac Myocytes.
Article in Cardiovascular drugs and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Myocardial Matrix Metalloproteinase 3 Protein Expression in Ischemic Heart Failure.International journal of molecular sciences · 2026Article
- Astragalus membranaceus injection activates mitophagy and protects mitochondrial function in chronic heart failure via inhibiting AKT/mTOR pathway.Scientific reports · 2025Article
- Furosemide Promotes Inflammatory Activation and Myocardial Fibrosis in Swine with Tachycardia-Induced Heart Failure.International journal of molecular sciences · 2025Article
- Mechanically and Chemically Defined PEG Hydrogels Improve Reproducibility in Human Cardioid Development.Advanced healthcare materials · 2025Article
- Involvement of ADAM17-Klotho Crosstalk in High Glucose-Induced Alterations of Podocyte Function.International journal of molecular sciences · 2025Article
- The Effects of Chronic Immunosuppressive Treatment on Morphological Changes in Cardiac Tissue and the Balance between Matrix Metalloproteinases (MMP-2 and MMP-9) and Their Inhibitors in the Rat Heart.International journal of molecular sciences · 2024Article
- Almost 50 Years of Monomeric Extracellular Ubiquitin (eUb).Pharmaceuticals (Basel, Switzerland) · 2024Review
- RNA-Binding Proteins as Critical Post-Transcriptional Regulators of Cardiac Regeneration.International journal of molecular sciences · 2023Review
- NaPharmaceuticals (Basel, Switzerland) · 2022Review
- Exploring Key Genes and Pathways of Cardiac Hypertrophy Based on Bioinformatics.Disease markers · 2022Article
- Pressure Overload Activates DNA-Damage Response in Cardiac Stromal Cells: A Novel Mechanism Behind Heart Failure With Preserved Ejection Fraction?Frontiers in cardiovascular medicine · 2022Article
- Levels of Serum sST2, MMP-3, and Gal-3 in Patients with Essential Hypertension and Their Correlation with Left Ventricular Hypertrophy.Evidence-based complementary and alternative medicine : eCAM · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeMatrix metalloproteinases (MMPs) are identified as modulators of the extracellular matrix in heart failure progression. However, evidence for intracellular effects of MMPs is emerging. Pro- and anti-hypertrophic cardiac effects are described. This may be due to the various sources of different MMPs in the heart tissue. Therefore, the aim of the present study was to determine the role of MMPs in hypertrophic growth of isolated rat ventricular cardiac myocytes.
methodsCardiomyocytes were isolated form ventricular tissues of the rat hearts by collagenase perfusion. RT-qPCR, western blots, and zymography were used for expression and MMP activity analysis. Cross-sectional area and the rate of protein synthesis were determined as parameters for hypertrophic growth.
resultsMMP-1, MMP-2, MMP-3, MMP-9 and MMP-14 mRNAs were detected in cardiomyocytes, and protein expression of MMP-2, MMP-9, and MMP-14 was identified. Hypertrophic stimulation of cardiomyocytes did not enhance, but interestingly decreased expression of MMPs, indicating that downregulation of MMPs may promote hypertrophic growth. Indeed, the nonselective MMP inhibitors TAPI-0 or TIMP2 and the MMP-2-selective ARP-100 enhanced hypertrophic growth. Furthermore, TAPI-0 increased phosphorylation and thus activation of extracellular signaling kinase (ERK) and Akt (protein kinase B), as well as inhibition of glycogen synthase 3β (GSK3β). Abrogation of MEK/ERK- or phosphatidylinositol-3-kinase(PI3K)/Akt/GSK3β-signaling with PD98059 or LY290042, respectively, inhibited hypertrophic growth under TAPI-0.
conclusionMMPs' inhibition promotes hypertrophic growth in cardiomyocytes in vitro. Therefore, MMPs in the healthy heart may be important players to repress cardiac hypertrophy.
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