Evidence map›Paper›PMID 41028611›Full record

ArticleAngiogenesis2025

Myocardial infarction induces endothelial dysfunction with independence of cardiovascular risk factors.

Francisco Rafael Jimenez-Trinidad, Núria Solanes, Marta Arrieta, Blanca Llonch, Mercè Roqué, Xavier Freixa, Salvatore Brugaletta, Luis Ortega-Paz, Juan José Rodríguez, Pedro Cepas-Guillen and 5 more

Abstract read
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In one paragraph

Article in Angiogenesis, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

15 authors.

Francisco Rafael Jimenez-Trinidad *Cardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Núria Solanes *Cardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Marta ArrietaCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Blanca LlonchCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Mercè RoquéCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Xavier FreixaCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Salvatore BrugalettaCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Luis Ortega-PazDivision of Cardiology, University of Florida College of Medicine, Jacksonville, FL, USA.
Juan José RodríguezCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Pedro Cepas-GuillenCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Gemma VilhaurResearch Institute-Sant Pau, Hospital de la Santa Creu i Sant Pau, IIB-Sant Pau, Barcelona, Spain.
Manel SabatéCardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Ana Paula Dantas *Cardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain.
Olga Tura-Ceide *Department of Pulmonary Medicine, Servei de Pneumologia, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Montserrat Rigol *Cardiology Department, Institut Clinic Cardiovascular (ICCV), Hospital Clinic, Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), School of Medicine and Health Sciences, University of Barcelona, Barcelona, Spain. mrigol@recerca.clinic.cat.

Funding

Instituto de Salud Carlos III PI18/00277Instituto de Salud Carlos III PI19/00264Ministerio de Ciencia e Innovación FPU19/04925Sociedad Española de Cardiología SEC/FECINV-BAS 20/012
6 · The paper itself

Abstract

aimsEndothelial dysfunction and impaired angiogenesis are hallmarks of ischemic heart disease and critical determinants of adverse cardiovascular outcomes after myocardial infarction (MI). While conventional cardiovascular risk factors (CVRFs) are known contributors, the specific role of MI itself triggering endothelial dysfunction remains unclear. This study aims to assess the direct impact of MI on endothelial function, independent of cardiovascular risk factors, using human and porcine endothelial colony-forming cells (ECFCs) as a surrogate cellular model. METHODS AND

resultsHuman ECFCs (hECFCs) were isolated from the peripheral blood of healthy volunteers (Control-hECFCs, n = 6), patients immediately after MI (AMI-hECFCs, n = 6), and patients 6 months after MI (CMI-hECFCs, n = 6). To evaluate the direct effect of MI independently of CVRFs, a porcine model was used: healthy pigs (n = 6) underwent 90 min of myocardial ischemia by coronary balloon occlusion followed by reperfusion. Porcine ECFCs (pECFCs) were isolated before MI (Control-pECFCs) and one month after MI (CMI-pECFCs, n = 6). In vitro, CMI-hECFCs and CMI-pECFCs had delayed colony formation, whereas AMI-hECFCs did not. Morphological alterations were observed in AMI-hECFCs and CMI-hECFCs (area and shape), while only shape changes were found in CMI-pECFCs. Senescence was increased in AMI-hECFCs and CMI-hECFCs, but not in CMI-pECFCs. Elevated oxidative stress was only detected in CMI-hECFCs. Functional angiogenic and proliferative capacities were reduced in AMI-hECFCs, CMI-hECFCs and CMI-pECFCs; however, only CMI-hECFCs and CMI-pECFCs displayed impaired migration. Molecular analysis showed overactivation of the MSK2/MKK3/p53 signalling axis in dysfunctional ECFCs, while synergistic inhibition of the axis partially restored ECFC function.

conclusionsMI induces sustained ECFC dysfunction independently of cardiovascular risk factors. Targeting the MSK2/MKK3/p53 pathway may be a promising therapeutic strategy to restore endothelial function and improve angiogenesis after MI.

Indexed as

Endothelial CellsEndothelium, VascularMyocardial InfarctionAgedAnimalsFemaleHeart Disease Risk FactorsHumansMaleMiddle AgedRisk FactorsSwineAngiogenesisEndothelial cellsMAPKMyocardial infarctionRisk factors

Identifiers

PMID41028611

What Socratic 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 Socratic graph.