ArticleArteriosclerosis, thrombosis, and vascular biology2025
Lymphatic Activation of ACKR3 Signaling Regulates Lymphatic Response After Ischemic Heart Injury.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
5 citing papers in PubMed.
- Cardiac lymphatic dysfunction and repair in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- β-Arrestin1/2 are essential for embryonic lymphatic vessel development.JCI insight · 2026Article
- Single-Cell Transcriptomics Reveals Dynamic Cellular Interactions and Molecular Mechanisms in Myocardial Infarction Recovery.International journal of genomics · 2026Article
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
- Molecular Mechanisms and Therapeutic Strategies Targeting Cardiac Lymphangiogenesis in Heart Failure.Cardiovascular toxicology · 2025Review
Corrections and comments
- Update of
Authors and funding
8 authors.
Funding
Abstract
backgroundIschemic heart disease is a prevalent cause of death and disability worldwide. Recent studies reported a rapid expansion of the cardiac lymphatic network upon ischemic heart injury and proposed that cardiac lymphatics may attenuate tissue edema and inflammatory mechanisms after ischemic heart injury. Nevertheless, the mechanisms through which hypoxic conditions affect cardiac lymphangiogenesis and function remain unclear. Here, we aimed to characterize the role of the AM (adrenomedullin) decoy receptor ACKR3 (atypical chemokine receptor-3) in the lymphatic response following ischemic heart injury.
methodsSpatial assessment of ACKR3 signaling in the heart after ischemic heart injury was conducted using ACKR3-Tango-GFP (green fluorescent protein) reporter mice. Roles of ACKR3 after ischemic heart injury were characterized in
resultsUsing the novel ACKR3-Tango-GFP reporter mice, we detected activation of ACKR3 signaling in cardiac lymphatics adjacent to the site of ischemic injury of left anterior descending artery ligation.
conclusionsLymphatic expression of ACKR3 governs numerous processes following ischemic heart injury, including the lymphangiogenic response, edema protection, and overall survival. These results expand our understanding of how the heart failure biomarker AM, regulated by lymphatic ACKR3, may exert its roles after ischemic cardiac injury.
Indexed as
Identifiers
What OpenQuestion holds
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.