ArticleCirculation. Heart failure2014
Mechanistic relationship between membrane type-1 matrix metalloproteinase and the myocardial response to pressure overload.
Article in Circulation. Heart failure, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- Plasma Biomarkers Reflecting Profibrotic Processes in Heart Failure With a Preserved Ejection Fraction: Data From the Prospective Comparison of ARNI With ARB on Management of Heart Failure With Preserved Ejection Fraction Study.Circulation. Heart failure · 2016Trial
- Hitting the Target! Challenges and Opportunities for TGF-β Inhibition for the Treatment of Cardiac fibrosis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Ubiquitin ligaseAmerican journal of physiology. Heart and circulatory physiology · 2021Article
- miR-133a Replacement Attenuates Thoracic Aortic Aneurysm in Mice.Journal of the American Heart Association · 2021Article
- From Systemic Inflammation to Myocardial Fibrosis: The Heart Failure With Preserved Ejection Fraction Paradigm Revisited.Circulation research · 2021Review
- Modulation of Cardiac Fibrosis in and Beyond Cells.Frontiers in molecular biosciences · 2021Review
- Leukocyte matrix metalloproteinase and tissue inhibitor gene expression patterns in children with primary hypertension.Journal of human hypertension · 2020Article
- Intrauterine Programming of Diabetes Induced Cardiac Embryopathy.Diabetes & obesity international journal · 2019Article
- Matrix metalloproteinase-14 is a biomarker of angiogenic activity in proliferative diabetic retinopathy.Molecular vision · 2018Article
- Systems biology-opportunities and challenges: the application of proteomics to study the cardiovascular extracellular matrix.Cardiovascular research · 2016Review
- Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling.Journal of molecular and cellular cardiology · 2016Review
- Pressure and Temperature Effects on the Activity and Structure of the Catalytic Domain of Human MT1-MMP.Biophysical journal · 2015Article
- Secreted protein acidic and rich in cysteine facilitates age-related cardiac inflammation and macrophage M1 polarization.American journal of physiology. Cell physiology · 2015Article
- Targeted overexpression of tissue inhibitor of matrix metalloproteinase-4 modifies post-myocardial infarction remodeling in mice.Circulation research · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlthough matrix metalloproteinases (MMPs) were initially thought to result primarily in extracellular matrix degradation, certain MMP types, such as membrane type-1 (MT1) MMP, may also be involved in profibrotic cascades through hydrolysis of latency-associated transforming growth factor-binding protein (LTBP-1) and activation of transforming growth factor-dependent profibrotic signaling. The present study tested the hypothesis that MT1-MMP plays a direct role in the matrix remodeling response to a left ventricular (LV) pressure overload (PO) stimulus. METHODS AND
resultsWild-type (WT) and transgenic mice with cardiac-restricted MT1-MMP overexpression or MT1-MMP reduced expression underwent PO for 4 weeks. PO resulted in a 57% increase in LV mass (no change in LV end diastolic volume, resulting in an increase in the LV mass/volume ratio consistent with concentric remodeling), a 60% increase in MT1-MMP-mediated LTBP-1 hydrolysis and a 190% increase in collagen content in WT mice. Although LV mass was similar among WT, MT1-MMP overexpression, and MT1-MMP reduced expression after PO, significant differences in LV function, MT1-MMP-mediated LTBP-1 hydrolysis, and collagen content occurred. PO in MT1-MMP overexpression increased LTBP-1 hydrolysis (18%), collagen content (60%), and left atrial dimension (19%; indicative of LV diastolic dysfunction) when compared with WT. PO in MT1-MMP reduced expression reduced left atrial dimension (19%), LTBP-1 hydrolysis (40%), and collagen content (32%) when compared with both WT.
conclusionsDespite an equivalent PO stimulus and magnitude of LV myocardial growth, altering MT1-MMP levels caused specific matrix-dependent changes in remodeling, thereby demonstrating a mechanistic role in the development of the maladaptive remodeling and myocardial fibrotic response to PO.
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Registered trials
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