ArticleAmerican journal of physiology. Heart and circulatory physiology2011
Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodeling.
Article in American journal of physiology. Heart and circulatory physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Cardiac Pericytes Acquire a Fibrogenic Phenotype and Contribute to Vascular Maturation After Myocardial Infarction.Circulation · 2023Article
- Remodeling and Fibrosis of the Cardiac Muscle in the Course of Obesity-Pathogenesis and Involvement of the Extracellular Matrix.International journal of molecular sciences · 2022Review
- Collagen denaturation in the infarcted myocardium involves temporally distinct effects of MT1-MMP-dependent proteolysis and mechanical tension.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Post-Myocardial Infarction Ventricular Remodeling Biomarkers-The Key Link between Pathophysiology and Clinic.Biomolecules · 2020Review
- Macrophages promote endothelial-to-mesenchymal transition via MT1-MMP/TGFβ1 after myocardial infarction.eLife · 2020Article
- Innate Immunity Effector Cells as Inflammatory Drivers of Cardiac Fibrosis.International journal of molecular sciences · 2020Review
- Cardioprotective Effect of Novel Matrix Metalloproteinase Inhibitors.International journal of molecular sciences · 2020Article
- Regulation of Myocardial Extracellular Matrix Dynamic Changes in Myocardial Infarction and Postinfarct Remodeling.Current cardiology reviews · 2020Review
- The Role of Macrophages in the Infarcted Myocardium: Orchestrators of ECM Remodeling.Frontiers in cardiovascular medicine · 2019Review
- Matrix metalloproteinase collagenolysis in health and disease.Biochimica et biophysica acta. Molecular cell research · 2017Review
- A Swine Model of Percutaneous Intracoronary Ethanol Induced Acute Myocardial Infarction and Ischemic Mitral Regurgitation.Journal of cardiovascular translational research · 2017Article
- The Processes and Mechanisms of Cardiac and Pulmonary Fibrosis.Frontiers in physiology · 2017Review
- Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.Journal of molecular and cellular cardiology · 2016Review
- Mechanisms of favorable effects of Rho kinase inhibition on myocardial remodeling and systolic function after experimental myocardial infarction in the rat.Therapeutic advances in cardiovascular disease · 2016Article
- Transient collagen triple helix binding to a key metalloproteinase in invasion and development.Structure (London, England : 1993) · 2015Article
- Targeted overexpression of tissue inhibitor of matrix metalloproteinase-4 modifies post-myocardial infarction remodeling in mice.Circulation research · 2014Article
- Mechanistic relationship between membrane type-1 matrix metalloproteinase and the myocardial response to pressure overload.Circulation. Heart failure · 2014Article
- Cyclosporin A in left ventricular remodeling after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2014Article
- Sick sinus syndrome induced by interferon and ribavirin therapy in a patient with chronic hepatitis C.Journal of cardiology cases · 2013Article
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
The membrane type 1 matrix metalloproteinase (MT1-MMP) is increased in left ventricular (LV) failure. However, the direct effects of altered MT1-MMP levels on survival, LV function, and geometry following myocardial infarction (MI) and the proteolytic substrates involved in this process remain unclear. MI was induced in mice with cardiac-restricted overexpression of MT1-MMP (MT1-MMPexp; full length human), reduced MT1-MMP expression (heterozygous; MT1-MMP(+/-)), and wild type. Post-MI survival was reduced with MT1-MMPexp and increased with MT1-MMP(+/-) compared with WT. LV ejection fraction was lower in the post-MI MT1-MMPexp mice compared with WT post-MI and was higher in the MT1-MMP(+/-) mice. In vivo localization of MT1-MMP using antibody-conjugated microbubbles revealed higher MT1-MMP levels post-MI, which were the highest in the MT1-MMPexp group and the lowest in the MT1-MMP(+/-) group. LV collagen content within the MI region was higher in the MT1-MMPexp vs. WT post-MI and reduced in the MT1-MMP(+/-) group. Furthermore, it was demonstrated that MT1-MMP proteolytically processed the profibrotic molecule, latency-associated transforming growth factor-1-binding protein (LTBP-1), and MT1-MMP-specific LTBP-1 proteolytic activity was increased by over fourfold in the post-MI MT1-MMPexp group and reduced in the MT1-MMP(+/-) group, which was directionally paralleled by phospho-Smad-3 levels, a critical signaling component of the profibrotic transforming growth factor pathway. We conclude that modulating myocardial MT1-MMP levels affected LV function and matrix structure, and a contributory mechanism for these effects is through processing of profibrotic signaling molecules. These findings underscore the diversity of biological effects of certain MMP types on the LV remodeling process.
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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.