ArticleProteomics. Clinical applications2016
Matrix metalloproteinase-9-dependent mechanisms of reduced contractility and increased stiffness in the aging heart.
Article in Proteomics. Clinical applications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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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.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Mass spectrometry reveals age-dependent collagen decline in murine atria.Annals of the New York Academy of Sciences · 2025Article
- Matrix Metalloproteinases: Pathophysiologic Implications and Potential Therapeutic Targets in Cardiovascular Disease.Biomolecules · 2025Review
- Influence of Ageing on the Pharmacodynamics and Pharmacokinetics of Chronically Administered Medicines in Geriatric Patients: A Review.Clinical pharmacokinetics · 2025Review
- Metalloproteinases (MMPs) in hypertensive disorders: role, function, pharmacology, and potential strategies to mitigate pathophysiological changes.Frontiers in pharmacology · 2025Review
- ColPTMScape: An open access knowledge base for tissue-specific collagen PTM maps.Matrix biology plus · 2024Article
- Considering impact of age and sex on cardiac cytoskeletal components.American journal of physiology. Heart and circulatory physiology · 2024Review
- miR-31-5p-Modified RAW 264.7 Macrophages Affect Profibrotic Phenotype of Lymphatic Endothelial Cells In Vitro.International journal of molecular sciences · 2022Article
- Comprehensive Mapping and Dynamics of Site-Specific Prolyl-Hydroxylation, Lysyl-Hydroxylation and Lysyl O-Glycosylation of Collagens Deposited in ECM During Zebrafish Heart Regeneration.Frontiers in molecular biosciences · 2022Article
- Regulators of cardiac fibroblast cell state.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- Cardiac tissue remodeling in healthy aging: the road to pathology.American journal of physiology. Cell physiology · 2020Review
- Cardiac changes associated with vascular aging.Clinical cardiology · 2020Review
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- The impact of aging on cardiac extracellular matrix.GeroScience · 2017Review
- Mechanical Regulation of Cardiac Aging in Model Systems.Circulation research · 2016Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
purposeMatrix metalloproteinases (MMPs) collectively degrade all extracellular matrix (ECM) proteins. Of the MMPs, MMP-9 has the strongest link to the development of cardiac dysfunction. Aging associates with increased MMP-9 expression in the left ventricle (LV) and reduced cardiac function. We investigated the effect of MMP-9 deletion on the cardiac ECM in aged animals. EXPERIMENTAL
designWe used male and female middle-aged (10- to16-month old) and old (20- to 24-month old) wild-type (WT) and MMP-9 null mice (n = 6/genotype/age). LVs were decellularized to remove highly abundant mitochondrial proteins that could mask identification of relative lower abundant components, analyzed by shotgun proteomics, and proteins of interest validated by immunoblot.
resultsElastin microfibril interface-located protein 1 (EMILIN-1) decreased with age in WT (p < 0.05), but not in MMP-9 null. EMILIN-1 promotes integrin-dependent cell adhesion and EMILIN-1 deficiency has been associated with vascular stiffening. Talin-2, a cytoskeletal protein, was elevated with age in WT (p < 0.05), and MMP-9 deficiency blunted this increase. Talin-2 is highly expressed in adult cardiac myocytes, transduces mechanical force to the ECM, and is activated by increases in substrate stiffness. Our results suggest that MMP-9 deletion may reduce age-related myocardial stiffness, which may explain improved cardiac function in MMP-9 null animals.
conclusionsWe identified age-related changes in the cardiac proteome that are MMP-9 dependent, suggesting MMP-9 as a possible therapeutic target for the aging patient.
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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.