ArticleCell communication and signaling : CCS2024
Tobacco smoke condensate-induced senescence in endothelial cells was ameliorated by colchicine treatment via suppression of NF-κB and MAPKs P38 and ERK pathways activation.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 23 citations in OpenAlex.
- Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.GeroScience · 2026Article
- Emerging multisystem disease mechanisms of e-cigarette vaping on human health.Toxicology reports · 2026Review
- SASP-driven vascular aging: unraveling the transcriptional nexus in endothelial senescence and cardiovascular disease.Histochemistry and cell biology · 2026Review
- Smoke Condensate-Induced Vascular Senescence and SASP Are Attenuated by Dual mTORC1/2 Inhibition with Rapalink-1.International journal of molecular sciences · 2026Article
- PI3K/mTOR inhibition attenuates cigarette smoke-induced senescence and SASP in oral fibroblasts: implications for tumor microenvironment remodeling.Frontiers in cell and developmental biology · 2026Article
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Cigarette Smoking as an Independent Predictor of Endothelial Cell Loss After Cataract Surgery: A Prospective Cohort Study.Clinical ophthalmology (Auckland, N.Z.) · 2026Article
- Network pharmacology and molecular docking to explore the potential mechanism of Codonopsis pilosula delaying aging.Medicine · 2025Article
- The Emerging Role of Senolysis in Atherosclerosis.Medicina (Kaunas, Lithuania) · 2025Review
- First Direct Evidence of Accelerated Molecular Aging in Intracranial Aneurysmal Tissue.Aging cell · 2025Article
- Platelet factor 4 and stromal cell-derived factor are novel prognostic biomarkers for cerebral vasospasm and mortality after subarachnoid hemorrhage.Scientific reports · 2025Article
- Aged Garlic Extract and Its Bioactive Molecules S-Allyl-Cysteine and S1-Propenyl-Cysteine: A Review Focusing on Evidences Supporting Their Use for Mitigating the Effects of Cigarette Smoking.Molecules (Basel, Switzerland) · 2025Review
- Factors associated with anti-drug antibody production in ankylosing spondylitis patients treated with the infliximab biosimilar CT-P13.Journal of rheumatic diseases · 2025Article
- Chronic Exposure to Two Regimens of Waterpipe Smoke Elicits Lung Injury, Genotoxicity, and Mitochondrial Impairment with the Involvement of MAPKs Activation in Mice.International journal of molecular sciences · 2025Article
- Xian Huang Fang Inhibits the PKCδ/MAPK Signaling Pathway to Attenuate Renal Tubular Epithelial Cell Senescence and Thereby Delay Renal Interstitial Fibrosis.Drug design, development and therapy · 2025Article
- Comprehensive Cellular Senescence Evaluation to Aid Targeted Therapies.Research (Washington, D.C.) · 2025Article
- Treatment of endothelial cell dysfunction in atherosclerosis: a new perspective integrating traditional and modern approaches.Frontiers in physiology · 2025Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Smoking is the major cause of cardiovascular diseases and cancer. It induces oxidative stress, leading to DNA damage and cellular senescence. Senescent cells increase the expression and release of pro-inflammatory molecules and matrix metalloproteinase, which are known to play a vital role in the initiation and progression of cardiovascular diseases and metastasis in cancer. The current study investigated the smoking induced cellular senescence and employed colchicine that blocked senescence in endothelial cells exposed to tobacco smoke condensate. Colchicine prevented oxidative stress and DNA damage in tobacco smoke-condensate-treated endothelial cells. Colchicin reduced β-gal activity, improved Lamin B1, and attenuated cell growth arrest markers P21 and P53. Colchicine also ameliorated the expression of SASP factors and inhibited the activation of NF-kB and MAPKs P38 and ERK. In summary, colchicine inhibited tobacco smoke condensate-induced senescence in endothelial cells by blocking the activation of NF-kB and MAPKs P38 and ERK.
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.