ArticleJournal of cellular and molecular medicine2020
Hyperlipidemia inhibits the protective effect of lisinopril after myocardial infarction via activation of dendritic cells.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Dendritic Cells in the Immunoregulation of Myocardial Infarction: Mechanisms and Therapeutic Strategies.Cardiovascular drugs and therapy · 2026Review
- Novel insights and an updated review of metabolic syndrome in immune-mediated organ transplant rejection.Frontiers in immunology · 2025Review
- JNK-dependent phosphorylation and nuclear translocation of EGR-1 promotes cardiomyocyte apoptosis.Apoptosis : an international journal on programmed cell death · 2022Article
- Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022Review
- Leukocyte-Mediated Cardiac Repair after Myocardial Infarction in Non-Regenerative vs. Regenerative Systems.Journal of cardiovascular development and disease · 2022Review
- Exploring the Impact of ACE Inhibition in Immunity and Disease.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2022Review
- Hyperlipidemia inhibits the protective effect of lisinopril after myocardial infarction via activation of dendritic cells.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the prevention of cardiac remodelling and inflammatory immune response after myocardial infarction (MI) via ACEI regulating dendritic cells (DCs), we explored whether the protective effect of ACEI was repressed under hyperlipidemic environment. In vivo, the survival rate and left ventricular function of the mice were recorded on day 7 after MI. Tissue samples of the myocardium, spleen, bone marrow and peripheral blood were assessed for Ang II concentration, inflammatory cytokines and DCs expression. In vitro, DCs were treated with ox-LDL + Ang II, simulating the internal environment of MI in ApoE
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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.