Evidence map›Paper›PMID 39775604›Full record

ArticlePloS one2024

Protective role of Pannexin1 in lymphatic endothelial cells in the progression of atherosclerosis in female mice.

Avigail Ehrlich, Graziano Pelli, Bernard Foglia, Filippo Molica, Brenda R Kwak

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Old drug with new application: spironolactone suppresses Panx 1-mediated CaInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Review
  3. Review
  4. Review
  5. Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Avigail EhrlichDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Graziano PelliDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Bernard FogliaDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Filippo MolicaDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.
Brenda R KwakDepartment of Pathology and Immunology, University of Geneva, Geneva, Switzerland.ORCID 0000-0003-0015-0044

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a progressive arterial disease arising from imbalanced lipid metabolism and a maladaptive immune response. The lymphatic system ensures tissue fluid homeostasis, absorption of dietary fats and trafficking of immune cells to draining lymph nodes, thereby potentially affecting atherogenesis. Endothelial cell-specific deletion of Pannexin1 (Panx1) in apolipoprotein E-deficient (Apoe-/-) mice increased atherosclerosis, suggesting a protective role for Panx1 channels in arterial endothelial function. Here, we investigated the role of Panx1 in lymphatic endothelial cells (LECs) in the initiation and the progression of atherosclerosis. Male or female Prox1-CreERT2+Panx1fl/flApoe-/- and Panx1fl/flApoe-/- mice were fed a high cholesterol diet (HCD) for 6 or 10 weeks. Tamoxifen-induced deletion of Panx1 was performed before or after 4 weeks of HCD. Body weight and serum lipid profiles were determined. The atherosclerotic plaque burden was assessed by Sudan-IV staining on thoracic-abdominal aortas and in aortic roots. Plaque composition was determined by immunohistochemistry. No differences in serum cholesterol, LDL and HDL were observed between genotypes and between sexes after HCD. Bodyweight, serum triglycerides and free fatty acid levels were higher before and after 6 weeks of HCD in male Prox1-CreERT2+Panx1fl/flApoe-/- and control Panx1fl/flApoe-/- mice compared to females of the same genotypes, which was associated with more lipids and inflammatory cells in their atherosclerotic plaques. In contrast, the atherosclerotic plaque burden was higher in female mice. The progression of atherosclerosis in male mice was not different between genotypes. However, female Prox1-CreERT2+Panx1fl/flApoe-/- mice showed enhanced progression of atherosclerosis compared to Panx1fl/flApoe-/- controls of the same sex. In addition, atherosclerotic lesions in female, but not in male, Prox1-CreERT2+Panx1fl/flApoe-/- mice showed T cell enrichment. Altogether, our results reveal differential sex-dependent effects of Panx1 in lymphatic endothelium on the progression of atherosclerosis.

Indexed as

AtherosclerosisConnexinsDisease ProgressionEndothelial CellsNerve Tissue ProteinsAnimalsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticConnexinsNerve Tissue ProteinsPanx1 protein, mouse

Identifiers

PMID39775604
PMCPMC11684638

What Socratic holds

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Registered trials

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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 Socratic graph.