ArticleMicroscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada2012
Matrix metalloproteinase-28 deletion amplifies inflammatory and extracellular matrix responses to cardiac aging.
Article in Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 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
- Correlation Between Plasma Matrix Metalloproteinase-28 Levels and Severity of Calcific Aortic Valve Stenosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Trial
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Unleashing the potential of exercise: conquering cardiovascular disease by targeting inflammasome activation.European journal of medical research · 2025Review
- The role of cardiac resident macrophage in cardiac aging.Aging cell · 2023Review
- Framing Heartaches: The Cardiac ECM and the Effects of Age.International journal of molecular sciences · 2023Review
- Immunomodulatory roles of metalloproteinases in rheumatoid arthritis.Frontiers in pharmacology · 2023Review
- Transcriptomic Characteristics Associated With Aging in the Thyroid Gland.Frontiers in nutrition · 2022Article
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Management of inflammation in cardiovascular diseases.Pharmacological research · 2021Review
- Matrix Metalloproteinases and Their Role in Mechanisms Underlying Effects of Quercetin on Heart Function in Aged Zucker Diabetic Fatty Rats.International journal of molecular sciences · 2021Article
- Exogenous IL-4 shuts off pro-inflammation in neutrophils while stimulating anti-inflammation in macrophages to induce neutrophil phagocytosis following myocardial infarction.Journal of molecular and cellular cardiology · 2020Article
- Circulating Matrix Metalloproteinase-28 Levels Are Related to GRACE Scores and Short-Term Outcomes in Patients with Acute Myocardial Infarction.BioMed research international · 2020Observational
- Extracellular matrix roles in cardiorenal fibrosis: Potential therapeutic targets for CVD and CKD in the elderly.Pharmacology & therapeutics · 2019Review
- MicroRNA-21 ablation exacerbates aldosterone-mediated cardiac injury, remodeling, and dysfunction.American journal of physiology. Endocrinology and metabolism · 2018Article
- The Mouse Heart Attack Research Tool 1.0 database.American journal of physiology. Heart and circulatory physiology · 2018Article
- LXR/RXR signaling and neutrophil phenotype following myocardial infarction classify sex differences in remodeling.Basic research in cardiology · 2018Article
- Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction.Translational research : the journal of laboratory and clinical medicine · 2018Review
- The impact of aging on cardiac extracellular matrix.GeroScience · 2017Review
- Matrix Metalloproteinases in Myocardial Infarction and Heart Failure.Progress in molecular biology and translational science · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
To determine if matrix metalloproteinase (MMP)-28 mediates cardiac aging, wild-type (WT) and MMP-28-/- young (7 ± 1 months, n = 9 each) and old (20 ± 2 months, n = 7 each) female mice were evaluated. MMP-28 expression in the left ventricle (LV) increased 42% in old WT mice compared to young controls (p < 0.05). By Doppler echocardiography, LV function declined at 20 ± 2 months of age for both groups. However, dobutamine stress responses were similar, indicating that cardiac reserve was maintained. Plasma proteomic profiling revealed that macrophage inflammatory protein (MIP)-1 α, MIP-1β and MMP-9 plasma levels did not change in WT old mice but were significantly elevated in MMP-28-/- old mice (all p < 0.05), suggestive of a higher inflammatory status when MMP-28 is deleted. RT2-PCR gene array and immunoblotting analyses demonstrated that MIP-1α and MMP-9 gene and protein levels in the LV were also higher in MMP-28-/- old mice (all p < 0.05). Macrophage numbers in the LV increased similarly in WT and MMP-28-/- old mice, compared to respective young controls (both p < 0.05). Collagen content was not different among the WT and MMP-28-/- young and old mice. In conclusion, LV inflammation increases with age, and MMP-28 deletion further elevates inflammation and extracellular matrix responses, without altering macrophage numbers or collagen content.
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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.