ArticleCirculation. Heart failure2009
Cardiac-restricted overexpression of membrane type-1 matrix metalloproteinase in mice: effects on myocardial remodeling with aging.
Article in Circulation. Heart failure, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- The interplay of senescence and MMPs in myocardial infarction: implications for cardiac aging and therapeutics.Biogerontology · 2025Review
- Post-Myocardial Infarction Ventricular Remodeling Biomarkers-The Key Link between Pathophysiology and Clinic.Biomolecules · 2020Review
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- Inhibitor of lysyl oxidase improves cardiac function and the collagen/MMP profile in response to volume overload.American journal of physiology. Heart and circulatory physiology · 2018Article
- Expression patterns of cardiac aging in Drosophila.Aging cell · 2017Article
- Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling.Journal of molecular and cellular cardiology · 2016Review
- The Aging Heart.Cold Spring Harbor perspectives in medicine · 2015Review
- Development of Radiolabeled Membrane Type-1 Matrix Metalloproteinase Activatable Cell Penetrating Peptide Imaging Probes.Molecules (Basel, Switzerland) · 2015Article
- Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries.Journal of molecular and cellular cardiology · 2015Review
- Cardiac-restricted overexpression or deletion of tissue inhibitor of matrix metalloproteinase-4: differential effects on left ventricular structure and function following pressure overload-induced hypertrophy.American journal of physiology. Heart and circulatory physiology · 2014Article
- Injectable and bioresponsive hydrogels for on-demand matrix metalloproteinase inhibition.Nature materials · 2014Article
- Mechanistic relationship between membrane type-1 matrix metalloproteinase and the myocardial response to pressure overload.Circulation. Heart failure · 2014Article
- Membrane-associated matrix proteolysis and heart failure.Circulation research · 2013Review
- Cardiac fibroblasts, fibrosis and extracellular matrix remodeling in heart disease.Fibrogenesis & tissue repair · 2012Article
- MT1-MMP-dependent remodeling of cardiac extracellular matrix structure and function following myocardial infarction.The American journal of pathology · 2012Article
- Pressure overload-dependent membrane type 1-matrix metalloproteinase induction: relationship to LV remodeling and fibrosis.American journal of physiology. Heart and circulatory physiology · 2012Article
- Biochemical role of the collagen-rich tumour microenvironment in pancreatic cancer progression.The Biochemical journal · 2012Review
- Direct regulation of membrane type 1 matrix metalloproteinase following myocardial infarction causes changes in survival, cardiac function, and remodeling.American journal of physiology. Heart and circulatory physiology · 2011Article
- MT1-MMP cooperates with Kras(G12D) to promote pancreatic fibrosis through increased TGF-β signaling.Molecular cancer research : MCR · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThe direct consequences of a persistently increased myocardial expression of the unique matrix metalloproteinase (MMP) membrane type-1 (MT1-MMP) on myocardial remodeling remained unexplored. METHODS AND
resultsCardiac-restricted MT1-MMPexp was constructed in mice using the full-length human MT1-MMP gene ligated to the myosin heavy chain promoter, which yielded approximately a 200% increase in MT1-MMP when compared with age/strain-matched wild-type (WT) mice. Left ventricular (LV) function and geometry was assessed by echocardiography in 3-month ("young") WT (n=32) and MT1-MMPexp (n=20) mice and compared with 14-month ("middle-aged") WT (n=58) and MT1-MMPexp (n=35) mice. LV end-diastolic volume was similar between the WT and MT1-MMPexp young groups, as was LV ejection fraction. In the middle-aged WT mice, LV end-diastolic volume and ejection fraction was similar to young WT mice. However, in the MT1-MMPexp middle-aged mice, LV end-diastolic volume was approximately 43% higher and LV ejection fraction 40% lower (both P<0.05). Moreover, in the middle-aged MT1-MMPexp mice, myocardial fibrillar collagen increased by nearly 2-fold and was associated with approximately 3-fold increase in the processing of the profibrotic molecule, latency-associated transforming growth factor binding protein. In a second study, 14-day survival after myocardial infarction was significantly lower in middle-aged MT1-MMPexp mice.
conclusionsPersistently increased myocardial MT1-MMP expression, in and of itself, caused LV remodeling, myocardial fibrosis, dysfunction, and reduced survival after myocardial injury. These findings suggest that MT1-MMP plays a mechanistic role in adverse remodeling within the myocardium.
Indexed as
Identifiers
What OpenQuestion holds
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.