ArticleFrontiers in pharmacology2020
The Anti-inflammatory Mediator Resolvin E1 Protects Mice Against Lipopolysaccharide-Induced Heart Injury.
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 80 citations in OpenAlex.
- Targeted Delivery of Specialized Pro-Resolving Mediators (SPMs) for Improved Treatments of Inflammatory Diseases and Cancer.Pharmaceutics · 2026Review
- MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.Molecular biology reports · 2026Article
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Analysis of PANoptosis-related genes in septic cardiomyopathy by bioinformatics, machine learning and experimental validation.Experimental and therapeutic medicine · 2026Article
- Hepatocyte-Specific GSDMD Deficiency Aggravates Sepsis by Disrupting Non-Canonical Secretion of Anti-Inflammatory Factors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Specialized Pro-Resolving Mediators as Emerging Players in Cardioprotection: From Inflammation Resolution to Therapeutic Potential.Acta physiologica (Oxford, England) · 2025Review
- Current anti-inflammatory strategies for treatment of heart failure: From innate to adaptive immunity.Pharmacological research · 2025Review
- A Cell Autonomous Free fatty acid receptor 4 - ChemR23 Signaling Cascade Protects Cardiac Myocytes from Ischemic Injury.bioRxiv : the preprint server for biology · 2025Article
- Molecular dynamics of inflammation resolution: therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Resolvin D2/GPR 18 axis ameliorates pressure overload-induced heart failure by inhibiting pro-inflammatory macrophage polarization.Journal of lipid research · 2024Article
- Carvacrol alleviates LPS-induced myocardial dysfunction by inhibiting the TLR4/MyD88/NF-κB and NLRP3 inflammasome in cardiomyocytes.Journal of inflammation (London, England) · 2024Article
- Crosstalk between macrophages and immunometabolism and their potential roles in tissue repair and regeneration.Heliyon · 2024Review
- Role for BLT1 in regulating inflammation within adipose tissue immune cells of aged mice.Immunity & ageing : I & A · 2024Article
- Cardiac macrophage metabolism in health and disease.Trends in endocrinology and metabolism: TEM · 2024Review
- Article
- Pharmacological effects of specialized pro-resolving mediators in sepsis-induced organ dysfunction: a narrative review.Frontiers in immunology · 2024Review
- Ferrostatin-1 improves acute sepsis-induced cardiomyopathy via inhibiting neutrophil infiltration through impaired chemokine axis.Frontiers in cell and developmental biology · 2024Article
- Macrophage neogenin deficiency exacerbates myocardial remodeling and inflammation after acute myocardial infarction through JAK1-STAT1 signaling.Cellular and molecular life sciences : CMLS · 2023Article
- Resolvin E1 heals injured cardiomyocytes: Therapeutic implications and H-FABP as a readout for cardiovascular disease & systemic inflammation.Prostaglandins, leukotrienes, and essential fatty acids · 2023Article
- IL-30 protects against sepsis-induced myocardial dysfunction by inhibiting pro-inflammatory macrophage polarization and pyroptosis.iScience · 2023Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSepsis-induced cardiomyopathy (
methodsC57BL/6J mice were randomly divided into three groups: control, lipopolysaccharide (LPS), and LPS + RvE1. Echocardiography, Western blotting (WB), quantitative real-time (QRT)-PCR, histological analyses, and flow cytometry were used to evaluate cardiac function, myocardial inflammation, and the underlying mechanisms.
resultsThe RvE1-injected group showed improved left ventricular (LV) function and reduced serum lactate dehydrogenase (LDH) and creatine kinase myocardial bound (CK-MB) levels. Compared to LPS treatment alone, RvE1 treatment inhibited the infiltration of neutrophils and macrophages into the heart and spleen and suppressed the secretion of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and monocyte chemoattractant protein (MCP)-1, in the heart. We also observed that the activation of the mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-κB signaling pathways was blocked by RvE1 treatment, and this inhibition contributed to the improvement in the inflammatory response induced by LPS. RvE1 inhibited LPS-induced M1 macrophage polarization and promoted macrophage polarization toward the M2-like phenotype in both the heart and spleen. In addition, LPS administration dysregulated cyclooxygenase (COX) and lipoxygenase (LOX) in the heart, which were rectified by RvE1 treatment. RvE1 also reduced myocardial apoptosis rate in response to LPS-induced heart injury.
conclusionRvE1 protects the heart against
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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.