ArticleThe American journal of pathology2005
Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
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Who cites it
65 citing papers in PubMed, 157 citations in OpenAlex.
- Targeting inflammation in heart failure-from genetic evidence to therapeutic agents.ESC heart failure · 2026Article
- Novel Drug Targets in Diastolic Heart Disease.International journal of molecular sciences · 2025Review
- The relationship between inflammatory factors and heart failure: evidence based on bidirectional Mendelian randomization analysis.Frontiers in cardiovascular medicine · 2024Article
- Fibrotic remodeling and tissue regeneration mechanisms define the therapeutic potential of human muscular progenitors.Bioengineering & translational medicine · 2023Article
- Treatment of cardiac fibrosis: from neuro-hormonal inhibitors to CAR-T cell therapy.Heart failure reviews · 2023Review
- Distinguishing Plasmin-Generating Microvesicles: Tiny Messengers Involved in Fibrinolysis and Proteolysis.International journal of molecular sciences · 2023Review
- Role of heparanase in ARDS through autophagy and exosome pathway (review).Frontiers in pharmacology · 2023Review
- The Remaining Conundrum of the Role of the NaReviews in cardiovascular medicine · 2022Review
- Dipeptide IF and Exercise Training Attenuate Hypertension in SHR Rats by Inhibiting Fibrosis and Hypertrophy and Activating AMPKα1, SIRT1, and PGC1α.International journal of molecular sciences · 2022Article
- Article
- Early IL-17A production helps establish Mycobacterium intracellulare infection in mice.PLoS pathogens · 2022Article
- Plasmin activity promotes amyloid deposition in a transgenic model of human transthyretin amyloidosis.Nature communications · 2021Article
- Reversion inducing cysteine rich protein with Kazal motifs and cardiovascular diseases: The RECKlessness of adverse remodeling.Cellular signalling · 2021Review
- Network model-based screen for FDA-approved drugs affecting cardiac fibrosis.CPT: pharmacometrics & systems pharmacology · 2021Article
- Fibrosis after Myocardial Infarction: An Overview on Cellular Processes, Molecular Pathways, Clinical Evaluation and Prognostic Value.Medical sciences (Basel, Switzerland) · 2021Review
- G Protein-Coupled Estrogen Receptor 30 Reduces Transverse Aortic Constriction-Induced Myocardial Fibrosis in Aged Female Mice by Inhibiting the ERK1/2 -MMP-9 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Innate Immune Cells in Pressure Overload-Induced Cardiac Hypertrophy and Remodeling.Frontiers in cell and developmental biology · 2021Review
- A Porcine Model of Heart Failure With Preserved Ejection Fraction Induced by Chronic Pressure Overload Characterized by Cardiac Fibrosis and Remodeling.Frontiers in cardiovascular medicine · 2021Article
- MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020Article
- Tenascin-C aggravates ventricular dilatation and angiotensin-converting enzyme activity after myocardial infarction in mice.ESC heart failure · 2020Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Left ventricular (LV) hypertrophy is a natural response of the heart to increased pressure loading, but accompanying fibrosis and dilatation may result in irreversible life-threatening heart failure. Matrix metalloproteinases (MMPs) have been invoked in various cardiac diseases, however, direct genetic evidence for a role of the plasminogen activator (PA) and MMP systems in pressure overload-induced LV hypertrophy and in heart failure is lacking. Therefore, the consequences of transverse aortic banding (TAB) were analyzed in mice lacking tissue-type PA (t-PA(-/-)), urokinase-type PA (u-PA(-/-)), or gelatinase-B (MMP-9(-/-)), and in wild-type (WT) mice after adenoviral gene transfer of the PA-inhibitor PAI-1 or the MMP-inhibitor TIMP-1. TAB elevated LV pressure comparably in all genotypes. In WT and t-PA(-/-) mice, cardiomyocyte hypertrophy was associated with myocardial fibrosis, LV dilatation and dysfunction, and pump failure after 7 weeks. In contrast, in u-PA(-/-) mice or in WT mice after PAI-1- and TIMP-1-gene transfer, cardiomyocyte hypertrophy was moderate and only minimally associated with cardiac fibrosis and LV dilatation, resulting in better preservation of pump function. Deficiency of MMP-9 had an intermediate effect. These findings suggest that the use of u-PA- or MMP-inhibitors might preserve cardiac pump function in LV pressure overloading.
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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.