ArticleAmerican journal of translational research2015
Knockdown of EMMPRIN improves adverse remodeling mediated by IL-18 in the post-infarcted heart.
Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
The trial behind it
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
5 citing papers in PubMed, 6 citations in OpenAlex.
- Progress of Research into the Interleukin-1 Family in Cardiovascular Disease.Journal of inflammation research · 2022Review
- Early Changes in Circulating Interleukins and Residual Inflammatory Risk After Acute Myocardial Infarction.Arquivos brasileiros de cardiologia · 2020Article
- Role of cytokines and inflammation in heart function during health and disease.Heart failure reviews · 2018Review
- Basigin rs8259 Polymorphism Confers Decreased Risk of Chronic Heart Failure in a Chinese Population.International journal of environmental research and public health · 2017Article
- Extracellular matrix metalloproteinase inducer enhances host resistance against pseudomonas aeruginosa infection through MAPK signaling pathway.American journal of translational research · 2016Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-18 (IL-18) exacerbates cardiac dysfunction following myocardial infarction (MI). Extracellular matrix metalloproteinase inducer (EMMPRIN) has been shown to exacerbate ventricular remodeling via induction of extracellular matrix metalloproteinase (MMP) synthesis. While up-regulation of EMMPRIN expression by IL-18 has been demonstrated in vitro, little is known regarding its in vivo effects. Here, we investigated the role of EMMPRIN in progressive post-infarct ventricular remodeling induced by IL-18. Cardiac function was impaired on echocardiography and organ weight was increased in mice receiving daily intraperitoneal injection of IL-18 following MI. Accompanying these adverse functional effect were increased EMMPRIN levels. Gene silencing of cardiac EMMPRIN by intramyocardial RNA interference rescued IL-18 mediated adverse effects on post-infarct cardiac function. Finally, EMMPRIN silencing reduced MMP-9 expression in the post-infarcted left ventricular myocardium. In conclusion, progressive post-infarct left ventricular remodeling induced by IL-18 can be reversed by gene silencing of EMMPRIN. Knock down of EMMPRIN may be a potential therapeutic strategy to abrogate the adverse effects of IL-18 on post-infarct left ventricular remodeling likely via MMP-9 inhibition.
Indexed as
Identifiers
26692934PMC4656767W2263596785What OpenQuestion holds
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.