ArticleInternational journal of molecular medicine2019
Bacterial lipopolysaccharide and antimicrobial LL-37 enhance ICAM-1 expression and NF-κB p65 phosphorylation in senescent endothelial cells.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 20 citations in OpenAlex.
- Sepsis-associated endothelial dysfunction: clinical phenotypes, biomarkers, bedside evidence, and translational implications.The Journal of clinical investigation · 2026Review
- Endothelial TLR4 at the Crossroads of Vascular Senescence and Targeted Senotherapeutics.Aging cell · 2026Review
- β-Amyloid (Aβ) and Human Cathelicidin LL-37: Two Sides of the Same Coin?International journal of molecular sciences · 2026Review
- Tooth Decay Promotes Senescence in Dental Pulp Stem Cells, Modifying Their Biological and Proteomic Profiles.Journal of cellular physiology · 2026Article
- Gut microbiota in Henoch-Schönlein purpura: from pathogenesis to therapeutic strategies.Frontiers in immunology · 2026Review
- The Emerging Role of Senolysis in Atherosclerosis.Medicina (Kaunas, Lithuania) · 2025Review
- Purinergic receptors in atherosclerosis: implications for pathophysiology and therapeutic strategies.Journal of physiology and biochemistry · 2025Review
- Cathelicidin: Insights into Its Impact on Metabolic Syndrome and Chronic Inflammation.Metabolites · 2024Review
- Gut Microbiome and Its Role in Valvular Heart Disease: Not a "Gutted" Relationship.Life (Basel, Switzerland) · 2024Review
- Cathelicidin boosts the antifungal activity of neutrophils and improves prognosis duringInfection and immunity · 2024Article
- Effect of artesunate on cardiovascular complications in periodontitis in a type I diabetes rat model and related mechanisms.Journal of endocrinological investigation · 2023Article
- Cathelicidin (LL-37) causes expression of inflammatory factors in coronary artery endothelial cells of Kawasaki disease by activating TLR4-NF-κB-NLRP3 signaling.Immunity, inflammation and disease · 2023Article
- Phytochemicals and Vitamin D for a Healthy Life and Prevention of Diseases.International journal of molecular sciences · 2023Review
- Gut Molecules in Cardiometabolic Diseases: The Mechanisms behind the Story.International journal of molecular sciences · 2023Review
- Role of antimicrobial peptide cathelicidin in thrombosis and thromboinflammation.Frontiers in immunology · 2023Review
- Metformin mitigates SASP secretion and LPS-triggered hyper-inflammation in Doxorubicin-induced senescent endothelial cells.Frontiers in aging · 2023Article
- A robust host-response-based signature distinguishes bacterial and viral infections across diverse global populations.Cell reports. Medicine · 2022Article
- Lipopolysaccharides and Cellular Senescence: Involvement in Atherosclerosis.International journal of molecular sciences · 2022Review
- HO-1 Upregulation by Kaempferol via ROS-Dependent Nrf2-ARE Cascade Attenuates Lipopolysaccharide-Mediated Intercellular Cell Adhesion Molecule-1 Expression in Human Pulmonary Alveolar Epithelial Cells.Antioxidants (Basel, Switzerland) · 2022Article
- Molecular Characterization and Expression Analysis of Intercellular Adhesion Molecule-1 (ICAM-1) Genes in Rainbow Trout (Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is associated with the induction of a proinflammatory phenotype. Notably, senescent endothelial cells are detected at the sites of atherosclerotic lesions, suggesting the involvement of senescent endothelial cells in atherogenesis. Moreover, bacterial infection has been speculated to contribute to the pathogenesis of atherosclerosis. The present study investigated the effects of Gram‑negative bacterial lipopolysaccharide (LPS) and LL‑37 (a human antimicrobial peptide of the cathelicidin family), on senescent endothelial cells, using serially passaged human endothelial cells. The results indicated that senescent endothelial cells exhibited the basal proinflammatory phenotype, as evidenced by higher intercellular adhesion molecule‑1 (ICAM‑1) expression and NF‑κB p65 phosphorylation, compared with non‑senescent cells. Additionally, exposure to LPS and LL‑37 further enhanced the expression of ICAM‑1 in senescent endothelial cells, compared with non‑senescent cells. Of note, the NF‑κB p65 pathway was more activated in senescent endothelial cells stimulated with LPS and LL‑37. Furthermore, the expression levels of the receptors for LPS and LL‑37 [toll‑like receptor 4 (TLR4) and purinergic receptor P2X 7 (P2X7), respectively] were upregulated in senescent endothelial cells. These observations indicated that LPS and LL‑37 enhanced the ICAM‑1 expression and NF‑κB p65 activation in senescent endothelial cells, potentially via the upregulated TLR4 and P2X7. Thus, senescent endothelial cells may contribute to the pathogenesis of atherosclerosis via the basal proinflammatory phenotype and the enhanced inflammatory responses against atherogenic factors, including LPS and LL‑37.
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.