ArticleJournal of the American Heart Association2026
Lymphatic Endothelial C-C Motif Chemokine Ligand 2 Enhances Lymphangiogenesis and Lymphatic Clearance of Macrophages Following Myocardial Infarction.
Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Lymphatic Endothelial Cells in Health and Disease.MedComm · 2026Review
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInflammatory responses are crucial in the pathological cardiac remodeling and tissue repair after myocardial infarction (MI). The lymphatic endothelial cells (LECs) significantly influence immune cell clearance and mitigate cardiac inflammation. Chemokines are known to tightly regulate immune cell mobilization within the infarcted heart, affecting both inflammation and remodeling. However, the role of chemokines expressed by LECs in the regulation of cardiac inflammation post MI remains unclear. Our study aimed to investigate whether LEC-expressing CCL2 (C-C motif chemokine ligand 2) regulated post-MI cardiac remodeling and its underlying molecular mechanisms.
methodsWe generated LEC-conditional
resultsOur results showed that the LEC-
conclusionsThis study reveals that cardiac LEC-expressing CCL2 tightly controls macrophage trafficking via lymphatic vessels in injured hearts and thus diminishes post-MI inflammatory responses and lessens adverse cardiac remodeling. Our findings suggest that modulating CCL2 signaling in LECs could provide a promising therapeutic target for resolving excessive inflammation and ameliorating adverse cardiac remodeling after MI.
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Registered trials
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