ArticleJournal of molecular and cellular cardiology2014
Aliskiren and valsartan mediate left ventricular remodeling post-myocardial infarction in mice through MMP-9 effects.
Article in Journal of molecular and cellular cardiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Renin-angiotensin system inhibitors mitigate radiation pneumonitis by activating ACE2-angiotensin-(1-7) axis via NF-κB/MAPK pathway.Scientific reports · 2023Article
- Non-invasive tragus stimulation improves cardiac post-ischemic remodeling by regulating cardiac parasympathetic activity.ESC heart failure · 2022Article
- Fibroblast mechanotransduction network predicts targets for mechano-adaptive infarct therapies.eLife · 2022Article
- Disparate effects of MMP and TIMP modulation on coronary atherosclerosis and associated myocardial fibrosis.Scientific reports · 2021Article
- Mechano-chemo signaling interactions modulate matrix production by cardiac fibroblasts.Matrix biology plus · 2021Article
- Infarct in the Heart: What's MMP-9 Got to Do with It?Biomolecules · 2021Review
- MAP Kinase Phosphatase-5 Deficiency Protects Against Pressure Overload-Induced Cardiac Fibrosis.Frontiers in immunology · 2021Article
- Does the Heart Want What It Wants? A Case for Self-Adapting, Mechano-Sensitive Therapies After Infarction.Frontiers in cardiovascular medicine · 2021Article
- Isolation Methods for Human CD34 Subsets Using Fluorescent and Magnetic Activated Cell Sorting: an In Vivo Comparative Study.Stem cell reviews and reports · 2020Article
- Macrophage Activities in Myocardial Infarction and Heart Failure.Cardiology research and practice · 2020Review
- The Mouse Heart Attack Research Tool 1.0 database.American journal of physiology. Heart and circulatory physiology · 2018Article
- Assigning matrix metalloproteinase roles in ischaemic cardiac remodelling.Nature reviews. Cardiology · 2018Review
- Article
- 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
- Aliskiren Improves Ischemia- and Oxygen Glucose Deprivation-Induced Cardiac Injury through Activation of Autophagy and AMP-Activated Protein Kinase.Frontiers in pharmacology · 2017Article
- Knowledge gaps to understanding cardiac macrophage polarization following myocardial infarction.Biochimica et biophysica acta · 2016Review
- Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution.Journal of molecular and cellular cardiology · 2016Article
- Proliferation and Recruitment Contribute to Myocardial Macrophage Expansion in Chronic Heart Failure.Circulation research · 2016Article
- MMP-9 signaling in the left ventricle following myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2016Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
We evaluated whether aliskiren, valsartan, or a combination of both was protective following myocardial infarction (MI) through effects on matrix metalloproteinase (MMP)-9. C57BL/6J wild type (WT, n=94) and MMP-9 null (null, n=85) mice were divided into 4 groups at 3h post-MI: saline (S), aliskiren (A; 50mg/kg/day), valsartan (V; 40mg/kg/day), or A+V and compared to no MI controls at 28days post-MI. All groups had similar infarct areas, and survival rates were higher in the null mice. The treatments influenced systolic function and hypertrophy index, as well as extracellular matrix (ECM) and inflammatory genes in the remote region, indicating that primary effects were on the viable myocardium. Saline treated WT mice showed increased end systolic and diastolic volumes and hypertrophy index, along with reduced ejection fraction. MMP-9 deletion improved LV function post-MI. Aliskiren attenuated the increase in end systolic volume and hypertrophy index, while valsartan improved end diastolic volumes and aliskiren+valsartan improved the hypertrophy index only when MMP-9 was absent. Extracellular matrix and inflammatory gene expression showed distinct patterns among the treatment groups, indicating a divergence in mechanisms of remodeling. This study shows that MMP-9 regulates aliskiren and valsartan effects in mice. These results in mice provide mechanistic insight to help translate these findings to post-MI patients.
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Registered trials
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