ArticleBritish journal of pharmacology2013
Reperfusion-induced myocardial dysfunction is prevented by endogenous annexin-A1 and its N-terminal-derived peptide Ac-ANX-A1(2-26).
Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 61 citations in OpenAlex.
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Inflammation and Resolution in Obesity-Related Cardiovascular Disease.International journal of molecular sciences · 2026Review
- Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1.Theranostics · 2026Article
- Failure to resolve inflammation contributes to juvenile onset cardiac damage in a mouse model of Duchenne muscular dystrophy.Cell death & disease · 2025Article
- ANXA1-FPR2 axis mitigates the susceptibility to atrial fibrillation in obesity via rescuing AMPK activity in response to lipid overload.Cardiovascular diabetology · 2024Article
- Integration of Microarray Data and Single-Cell Sequencing Analysis to Explore Key Genes Associated with Macrophage Infiltration in Heart Failure.Journal of inflammation research · 2024Article
- Anti-Inflammatory and Pro-Resolving Actions of the N-Terminal Peptides Ac2-26, Ac2-12, and Ac9-25 of Annexin A1 on Conjunctival Goblet Cell Function.The American journal of pathology · 2023Article
- Article
- Formylpeptide receptor 2: Nomenclature, structure, signalling and translational perspectives: IUPHAR review 35.British journal of pharmacology · 2022Review
- Annexin-A1: The culprit or the solution?Immunology · 2022Review
- Annexins and cardiovascular diseases: Beyond membrane trafficking and repair.Frontiers in cell and developmental biology · 2022Review
- Identification of Immune-Related Genes in Patients with Acute Myocardial Infarction Using Machine Learning Methods.Journal of inflammation research · 2022Article
- Ac2-26 mitigated acute respiratory distress syndrome rats via formyl peptide receptor pathway.Annals of medicine · 2021Article
- Regulation of Inflammation and Oxidative Stress by Formyl Peptide Receptors in Cardiovascular Disease Progression.Life (Basel, Switzerland) · 2021Review
- Pro-Resolving Mediator Annexin A1 Regulates Intracellular CaFrontiers in immunology · 2021Article
- Untangling Local Pro-Inflammatory, Reparative, and Regulatory Damage-Associated Molecular-Patterns (DAMPs) Pathways to Improve Transplant Outcomes.Frontiers in immunology · 2021Review
- Annexin-A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin-resistant, but not insulin-deficient, mice.British journal of pharmacology · 2020Article
- The Novel Small-molecule Annexin-A1 Mimetic, Compound 17b, Elicits Vasoprotective Actions in Streptozotocin-induced Diabetic Mice.International journal of molecular sciences · 2020Article
- Therapeutic Potential of Lipoxin AACS pharmacology & translational science · 2020Review
- Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway.Mediators of inflammation · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeAnnexin-A1 (ANX-A1) is an endogenous, glucocorticoid-regulated anti-inflammatory protein. The N-terminal-derived peptide Ac-ANX-A1(2-26) preserves cardiomyocyte viability, but the impact of ANX-A1-peptides on cardiac contractility is unknown. We now test the hypothesis that ANX-A1 preserves post-ischaemic recovery of left ventricular (LV) function. EXPERIMENTAL APPROACH: Ac-ANX-A1(2-26) was administered on reperfusion, to adult rat cardiomyocytes as well as hearts isolated from rats, wild-type mice and mice deficient in endogenous ANX-A1 (ANX-A1(-/-)). Myocardial viability and recovery of LV function were determined. KEY
resultsIschaemia-reperfusion markedly impaired both cardiomyocyte viability and recovery of LV function by 60%. Treatment with exogenous Ac-ANX-A1(2-26) at the onset of reperfusion prevented cardiomyocyte injury and significantly improved recovery of LV function, in both intact rat and wild-type mouse hearts. Ac-ANX-A1(2-26) cardioprotection was abolished by either formyl peptide receptor (FPR)-nonselective or FPR1-selective antagonists, Boc2 and cyclosporin H, but was relatively insensitive to the FPR2-selective antagonist QuinC7. ANX-A1-induced cardioprotection was associated with increased phosphorylation of the cell survival kinase Akt. ANX-A1(-/-) exaggerated impairment of post-ischaemic recovery of LV function, in addition to selective LV FPR1 down-regulation. CONCLUSIONS AND IMPLICATIONS: These data represent the first evidence that ANX-A1 affects myocardial function. Our findings suggest ANX-A1 is an endogenous regulator of post-ischaemic recovery of LV function. Furthermore, the ANX-A1-derived peptide Ac-ANX-A1(2-26) on reperfusion rescues LV function, probably via activation of FPR1. ANX-A1-based therapies may thus represent a novel clinical approach for the prevention and treatment of myocardial reperfusion injury.
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