ArticleCardiovascular research2012
Matrix metalloproteinase-9 deletion attenuates myocardial fibrosis and diastolic dysfunction in ageing mice.
Article in Cardiovascular research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 1 of them a synthesis that pooled it.
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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
111 citing papers in PubMed, 1 synthesis or guideline pooled it, 172 citations in OpenAlex.
- Matrix Metalloproteinases and Tissue Inhibitors of Metalloproteinases in Extracellular Matrix Remodeling during Left Ventricular Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2020Pooled it
- Young Mice Exhibit Increased Relative Ventricular Remodeling After AMI-A Longitudinal CMR Study.Aging cell · 2026Article
- Matrix Metalloproteinases and Cardiac Remodelling in Smokers with Acute Coronary Syndrome.International journal of molecular sciences · 2026Article
- The role of mitochondrial dysfunction, oxidative stress, and gender in cardiac fibrosis and vascular remodeling in an induced aged rat model with possible mitigation by eugenol nano-emulsion.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- From bump to pump: extracellular matrix remodeling, dynamics, and biomechanics in the maternal heart.American journal of physiology. Heart and circulatory physiology · 2026Review
- Geniposide Attenuates Post-Myocardial Infarction Cardiac RemodelingCurrent medicinal chemistry · 2026Article
- Acute binge alcohol increases risk of arrhythmias and myocardial fibrosis in a mouse model of arrhythmogenic cardiomyopathy.American journal of physiology. Heart and circulatory physiology · 2025Article
- Prolonged intermittent hypoxia accelerates cardiovascular aging and mortality: insights from a murine model of OSA.npj aging · 2025Article
- The cardiovascular consequences of chronic sleep fragmentation: Evidence from experimental models of obstructive sleep apnea.Sleep medicine · 2025Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- Multiparity induces persistent myocardial structural, functional and transcriptomic remodelling in mice.Scientific reports · 2025Article
- Mass spectrometry reveals age-dependent collagen decline in murine atria.Annals of the New York Academy of Sciences · 2025Article
- The interplay of senescence and MMPs in myocardial infarction: implications for cardiac aging and therapeutics.Biogerontology · 2025Review
- Endothelial oestrogen-myocardial cyclic guanosine monophosphate axis critically determines angiogenesis and cardiac performance during pressure overload.Cardiovascular research · 2024Article
- At the heart of inflammation: Unravelling cardiac resident macrophage biology.Journal of cellular and molecular medicine · 2024Review
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- The Senescent Heart-"Age Doth Wither Its Infinite Variety".International journal of molecular sciences · 2024Review
- Pharmacological mechanisms by which baicalin ameliorates cardiovascular disease.Frontiers in pharmacology · 2024Review
- Review
- Effects of RAGE Deletion on the Cardiac Transcriptome during Aging.International journal of molecular sciences · 2022Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
aimsAge-related diastolic dysfunction has been attributed to an increased passive stiffness, which is regulated by extracellular matrix (ECM). We recently showed that matrix metalloproteinase (MMP)-9, an ECM mediator, increases in the left ventricle (LV) with age. The aim of this study, accordingly, was to determine the role of MMP-9 in cardiac ageing. METHODS AND
resultsWe compared LV function in young (6-9 months), middle-aged (12-15 months), old (18-24 months) and senescent (26-34 months) wild-type (WT) and MMP-9 null mice (n ≥ 12/group). All groups had similar fractional shortenings and aortic peak velocities, indicating that systolic function was not altered by ageing or MMP-9 deletion. The mitral ratios of early to late diastolic filling velocities were reduced in old and senescent WT compared with young controls, and this reduction was attenuated in MMP-9 null mice. Concomitantly, the increase in LV collagen content was reduced in MMP-9 null mice (n = 5-6/group). To dissect the mechanisms of these changes, we evaluated the mRNA expression levels of 84 ECM and adhesion molecules by real-time qPCR (n = 6/group). The expression of pro-fibrotic periostin and connective tissue growth factor (CTGF) increased with senescence, as did transforming growth factor-β (TGF-β)-induced protein levels and Smad signalling, and these increases were blunted by MMP-9 deletion. In senescence, MMP-9 deletion also resulted in a compensatory increase in MMP-8.
conclusionMMP-9 deletion attenuates the age-related decline in diastolic function, in part by reducing TGF-β signalling-induced periostin and CTGF expression and increasing MMP-8 expression to regulate myocardial collagen turnover and deposition.
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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.