ArticleBasic research in cardiology2013
5-Lipoxygenase facilitates healing after myocardial infarction.
Article in Basic research in cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Post-myocardial Infarction Cardiac Remodeling: Multidimensional Mechanisms and Clinical Prospects of Stem Cell Therapy.Stem cell reviews and reports · 2025Review
- Impact of Reperfusion on Plasma Oxylipins in ST-Segment Elevation Myocardial Infarction.Metabolites · 2023Article
- Extrinsic and intrinsic modulators of inflammation-resolution signaling in heart failure.American journal of physiology. Heart and circulatory physiology · 2023Review
- Metabolic changes of glycerophospholipids during the reparative phase after myocardial infarction injury.Frontiers in cardiovascular medicine · 2023Article
- Arachidonate 5-lipoxygenase is essential for biosynthesis of specialized pro-resolving mediators and cardiac repair in heart failure.American journal of physiology. Heart and circulatory physiology · 2022Article
- Macrophages in myocardial infarction.American journal of physiology. Cell physiology · 2022Review
- Review
- Cells of the Immune System in Cardiac Remodeling: Main Players in Resolution of Inflammation and Repair After Myocardial Infarction.Frontiers in immunology · 2021Review
- Validation of diagnostic criteria and histopathological characterization of cardiac rupture in the mouse model of nonreperfused myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2020Article
- The Dynamic Interplay Between Cardiac Inflammation and Fibrosis.Frontiers in physiology · 2020Review
- Early increase of specialized pro-resolving lipid mediators in patients with ST-elevation myocardial infarction.EBioMedicine · 2019Article
- Genetic variation in the leukotriene pathway is associated with myocardial infarction in the Chinese population.Lipids in health and disease · 2019Article
- Genetic deletion of 12/15 lipoxygenase promotes effective resolution of inflammation following myocardial infarction.Journal of molecular and cellular cardiology · 2018Article
- Splenic leukocytes define the resolution of inflammation in heart failure.Science signaling · 2018Article
- Analysis of the dynamic co-expression network of heart regeneration in the zebrafish.Scientific reports · 2016Article
- Cardiomyocyte-specific Bmal1 deletion in mice triggers diastolic dysfunction, extracellular matrix response, and impaired resolution of inflammation.American journal of physiology. Heart and circulatory physiology · 2015Article
- Resolvin D1 activates the inflammation resolving response at splenic and ventricular site following myocardial infarction leading to improved ventricular function.Journal of molecular and cellular cardiology · 2015Article
- Obesity superimposed on aging magnifies inflammation and delays the resolving response after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2015Article
- Fibroblasts in myocardial infarction: a role in inflammation and repair.Journal of molecular and cellular cardiology · 2014Review
- Reoxygenation-derived toxic reactive oxygen/nitrogen species modulate the contribution of bone marrow progenitor cells to remodeling after myocardial infarction.Journal of the American Heart Association · 2014Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Early healing after myocardial infarction (MI) is characterized by a strong inflammatory reaction. Most leukotrienes are pro-inflammatory and are therefore potential mediators of healing and remodeling after myocardial ischemia. The enzyme 5-lipoxygenase (5-LOX) has a key role in the transformation of arachidonic acid in leukotrienes. Thus, we tested the effect of 5-LOX on healing after MI. After chronic coronary artery ligation, early mortality was significantly increased in 5-LOX(-/-) when compared to matching wildtype (WT) mice due to left ventricular rupture. This effect could be reproduced in mice treated with the 5-LOX inhibitor Zileuton. A perfusion mismatch due to the vasoactive potential of leukotrienes is not responsible for left ventricular rupture since local blood flow assessed by magnetic resonance perfusion measurements was not different. However, after MI, there was an accentuation of the inflammatory reaction with an increase of pro-inflammatory macrophages. Yet, mortality was not changed in chimeric mice (WT vs. 5-LOX(-/-) bone marrow in 5-LOX(-/-) animals), indicating that an altered function of 5-LOX(-/-) inflammatory cells is not responsible for the phenotype. Collagen production and accumulation of fibroblasts were significantly reduced in 5-LOX(-/-) mice in vivo after MI. This might be due to an impaired migration of 5-LOX(-/-) fibroblasts, as shown in vitro to serum. In conclusion, a lack or inhibition of 5-LOX increases mortality after MI because of healing defects. This is not mediated by a change in local blood flow, but through an altered inflammation and/or fibroblast function.
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