ArticleAmerican journal of physiology. Heart and circulatory physiology2022
Arachidonate 5-lipoxygenase is essential for biosynthesis of specialized pro-resolving mediators and cardiac repair in heart failure.
Article in American journal of physiology. Heart and circulatory physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
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- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Specialized pro-resolving mediators in myocardial infarction: orchestrators of inflammation resolution and tissue repair.Frontiers in cardiovascular medicine · 2026Review
- Resolution Pharmacology: State-of-the-art and therapeutic landscape.Pharmacological reviews · 2025Review
- Inflammation-resolution signalling in cardiac repair, remodelling, and heart failure.European heart journal open · 2025Review
- Spatial Transcriptomics Reveals Distinct Architectures but Shared Vulnerabilities in Primary and Metastatic Liver Tumors.Cancers · 2025Article
- Macro- and microinjury define the heart failure progression after permanent coronary ligation or ischemia-reperfusion in young healthy mice.American journal of physiology. Heart and circulatory physiology · 2025Article
- Intervention of machine learning in bladder cancer research using multi-omics datasets: systematic review on biomarker identification.Discover oncology · 2025Review
- Roles of Lipoxygenases in Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Enhanced Production of Lipid Mediators in Plasma and Activation of DNA Damage Pathways in PBMCs Are Correlated With the Severity of Ancestral SARS-CoV-2 Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
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- Subepicardial adipose genes contribute to the deterioration of heart failure preserved ejection fraction.Frontiers in cardiovascular medicine · 2025Article
- Specialized pro-resolving mediators in vascular inflammation and atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2024Review
- G protein subunit GeLife · 2024Article
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- Macrophage-driven cardiac inflammation and healing: insights from homeostasis and myocardial infarction.Cellular & molecular biology letters · 2023Review
- Genetic deletion of 12/15 lipoxygenase delays vascular remodeling and limits cardiorenal dysfunction after pressure overload.Journal of molecular and cellular cardiology plus · 2023Article
- Extrinsic and intrinsic modulators of inflammation-resolution signaling in heart failure.American journal of physiology. Heart and circulatory physiology · 2023Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Arachidonate 5-lipoxygenase (ALOX5)-derived leukotrienes are primary signals of leukocyte activation and inflammation in response to ischemic cardiac injury (MI; myocardial infarction). Using risk-free male C57BL/6J and ALOX5-null mice (8-12 wk), we quantitated leukocytes and ALOX5-derived bioactive lipids of the infarcted left ventricle (LV) and spleen to measure the physiological inflammation and cardiac repair. Our results showed that ALOX5 endogenously generates specialized pro-resolving mediators (SPMs) that facilitate cardiac repair post-MI. Deficiency of ALOX5 leads to increase in cyclooxygenase gene expression, 6-keto prostaglandin F1α, and delayed neutrophil clearance with signs of unresolved inflammation post-MI. Consequently, ALOX5 deficiency impaired the resolution of inflammation and cardiac repair, including increased myocardium rupture post-MI in acute heart failure. On-time ALOX5 activation is critical for leukocyte clearance from the infarcted heart, indicating an essential role of ALOX5 in the resolution of inflammation. In addition, to balance the inflammatory responses, ALOX5 is also necessary for fibroblast signaling, as the ALOX5-deficient fibroblast are prone to fibroblast-to-myofibroblast differentiation leading to defective scar formation in post-MI cardiac repair. Consistent with these findings, ALOX5-null mice showed an overly inflammatory response, defective fibrotic signaling, and unresolved inflammation. These findings are indicative of a critical role of ALOX5 in myocardium healing, inflammation-resolution signaling, cardiac repair, and fibroblast pathophysiology.
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Registered trials
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