ArticleCirculation research2014
Targeted overexpression of tissue inhibitor of matrix metalloproteinase-4 modifies post-myocardial infarction remodeling in mice.
Article in Circulation research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 44 citations in OpenAlex.
- RNA Therapeutics in Heart Failure.Journal of cardiovascular translational research · 2025Review
- Retrospective study on the short-term efficacy of different doses of Spironolactone in patients with heart failure of ischemic cardiomyopath and the influence of ventricular remodeling markers.American journal of cardiovascular disease · 2024Article
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
- Silencing RNA for MMPs May Be Utilized for Cardioprotection.Cardiovascular therapeutics · 2022Article
- Ezh2 Inhibits Replicative Senescence of Atrial Fibroblasts Through Promotion of H3K27me3 in the Promoter Regions of CDKN2a and Timp4 Genes.Journal of inflammation research · 2022Article
- MicroRNA-146b-5p promotes atrial fibrosis in atrial fibrillation by repressing TIMP4.Journal of cellular and molecular medicine · 2021Article
- A combined biomarker approach for characterising extracellular matrix profiles in acute myocardial infarction.Scientific reports · 2021Article
- Modulation of Cardiac Fibrosis in and Beyond Cells.Frontiers in molecular biosciences · 2021Review
- Effects of High-Dose Rosuvastatin on Ventricular Remodelling and Cardiac Function in ST-Segment Elevation Myocardial Infarction.Drug design, development and therapy · 2020Article
- Application of Hybrid Matrix Metalloproteinase-Targeted and DynamicCirculation. Cardiovascular imaging · 2019Article
- Primary cilia defects causing mitral valve prolapse.Science translational medicine · 2019Article
- Delivery of a matrix metalloproteinase-responsive hydrogel releasing TIMP-3 after myocardial infarction: effects on left ventricular remodeling.American journal of physiology. Heart and circulatory physiology · 2018Article
- Matrix metalloproteinase-2 knockout prevents angiotensin II-induced vascular injury.Cardiovascular research · 2017Article
- Sustained Release of a Peptide-Based Matrix Metalloproteinase-2 Inhibitor to Attenuate Adverse Cardiac Remodeling and Improve Cardiac Function Following Myocardial Infarction.Biomacromolecules · 2017Article
- Pregestational type 2 diabetes mellitus induces cardiac hypertrophy in the murine embryo through cardiac remodeling and fibrosis.American journal of obstetrics and gynecology · 2017Article
- Epigenetic silencing of TIMP4 in heart failure.Journal of cellular and molecular medicine · 2016Article
- Can heart function lost to disease be regenerated by therapeutic targeting of cardiac scar tissue?Seminars in cell & developmental biology · 2016Review
- Lung-specific RNA interference of coupling factor 6, a novel peptide, attenuates pulmonary arterial hypertension in rats.Respiratory research · 2016Article
- EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction.Theranostics · 2016Article
- Recent Developments in Heart Failure.Circulation research · 2015Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleMyocardial infarction (MI) causes an imbalance between matrix metalloproteinases and tissue inhibitors of matrix metalloproteinases (TIMPs) and is associated with adverse left ventricular (LV) remodeling. A uniform reduction in TIMP-4 post-MI has been observed.
objectiveTo examine post-MI remodeling with cardiac-restricted overexpression of TIMP-4, either through a transgenic or viral delivery approach. METHODS AND
resultsMI was induced in mice and then randomized to targeted injection of an adenoviral construct (10 μL; 8×10(9) plaque forming units/mL) encoding green fluorescent protein (GFP) and the full-length human TIMP-4 (Ad-GFP-TIMP4) or GFP. A transgenic construct with cardiac-restricted overexpression TIMP-4 (hTIMP-4exp) was used in a parallel set of studies. LV end-diastolic volume, an index of LV remodeling, increased by >60% from baseline at 5 days post-MI and by >100% at 21 days post-MI in the Ad-GFP only group. However, LV dilation was reduced by ≈50% in both the Ad-GFP-TIMP4 and hTIMP-4exp groups at these post-MI time points. LV ejection fraction was improved with either Ad-GFP-TIMP-4 or hTIMP-4exp. Fibrillar collagen expression and content were increased within the MI region with both TIMP-4 interventions, suggestive of matrix stabilization.
conclusionsThis study is the first to demonstrate that selective myocardial targeting for TIMP-4 induction through either a viral or transgenic approach favorably altered the course of adverse LV remodeling post-MI. Thus, localized induction of endogenous matrix metalloproteinase inhibitors, such as TIMP-4, holds promise as a means to interrupt the progression of post-MI remodeling.
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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.