Evidence map›Paper›PMID 26941847›Full record

ArticleTheranostics2016

EMMPRIN-Targeted Magnetic Nanoparticles for In Vivo Visualization and Regression of Acute Myocardial Infarction.

Irene Cuadrado, Maria Jose Garcia Miguel Piedras, Irene Herruzo, Maria Del Carmen Turpin, Borja Castejón, Paula Reventun, Ana Martin, Marta Saura, Jose Luis Zamorano, Carlos Zaragoza

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 53 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Irene Cuadrado1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Maria Jose Garcia Miguel Piedras1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Irene Herruzo1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Maria Del Carmen Turpin1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Borja Castejón1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Paula Reventun2. Department of Physiology, University of Alcalá, School of Medicine. Ctra. Madrid Barcelona, Km 3,300. 28875 Alcalá de Henares, Madrid, Spain.
Ana Martin1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Marta Saura2. Department of Physiology, University of Alcalá, School of Medicine. Ctra. Madrid Barcelona, Km 3,300. 28875 Alcalá de Henares, Madrid, Spain.
Jose Luis Zamorano1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Carlos Zaragoza1. Cardiology Department. University Francisco de Vitoria/Hospital Ramón y Cajal. Ctra. Colmenar Viejo, km. 9100. 28034 Madrid, Spain.
Instituto Cajal · ESUniversidad de Alcalá · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledInhibition of extracellular matrix (ECM) degradation may represent a mechanism for cardiac protection against ischemia. Extracellular matrix metalloproteinase inducer (EMMPRIN) is highly expressed in response to acute myocardial infarction (AMI), and induces activation of several matrix metalloproteinases (MMPs), including gelatinases MMP-2 and MMP-9. We targeted EMMPRIN with paramagnetic/fluorescent micellar nanoparticles conjugated with the EMMPRIN binding peptide AP-9 (NAP9), or an AP-9 scrambled peptide as a negative control (NAPSC). We found that NAP9 binds to endogenous EMMPRIN in cultured HL1 myocytes and in mouse hearts subjected to ischemia/reperfusion (IR). Injection of NAP9 at the time of or one day after IR, was enough to reduce progression of myocardial cell death when compared to CONTROL and NAPSC injected mice (infarct size in NAP9 injected mice: 32%±6.59 vs CONTROL: 46%±9.04 or NAPSC injected mice: 48%±7.64). In the same way, cardiac parameters were recovered to almost healthy levels (LVEF NAP9 63% ± 7.24 vs CONTROL 42% ± 4.74 or NAPSC 39% ± 6.44), whereas ECM degradation was also reduced as shown by inhibition of MMP-2 and MMP-9 activation. Cardiac magnetic resonance (CMR) scans have shown a signal enhancement in the left ventricle of NAP9 injected mice with respect to non-injected, and to mice injected with NAPSC. A positive correlation between CMR enhancement and Evans-Blue/TTC staining of infarct size was calculated (R:0.65). Taken together, these results point to EMMPRIN targeted nanoparticles as a new approach to the mitigation of ischemic/reperfusion injury.

Indexed as

MagneticsAnimalsBasiginDisease Models, AnimalHumansMiceMyocardial InfarctionNanoparticlesProtease InhibitorsTreatment OutcomeBasiginProtease InhibitorsAP9.EMMPRINIschemia/ReperfusionMatrix metalloproteinasesnanoparticles

Identifiers

PMID26941847
PMCPMC4775864
OpenAlexW2324055247

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.