Evidence map›Paper›PMID 38001470›Full record

ArticleJournal of inflammation (London, England)2023

Colchicine prevents oxidative stress-induced endothelial cell senescence via blocking NF-κB and MAPKs: implications in vascular diseases.

Huakang Zhou, Dilaware Khan, Sajid Muhammad Hussain, Norbert Gerdes, Carsten Hagenbeck, Majeed Rana, Jan Frederick Cornelius, Sajjad Muhammad

Open access · goldAbstract read
In one paragraph

Article in Journal of inflammation (London, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.1field-weighted citation impact, top 4% of its field
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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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  18. [Colchicine-Phoenix from the ashes].Wiener klinische Wochenschrift · 2025
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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

8 authors at 3 institutions in 3 countries.

Huakang ZhouDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany.
Dilaware KhanDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany. Dilaware.Khan@med.uni-duesseldorf.de.
Sajid Muhammad HussainCologne Center for Genomics (CCG), University of Cologne, Weyertal 115b, 50931, Cologne, Germany.
Norbert GerdesDivision of Cardiology, Pulmonology and Vascular Medicine, Medical Faculty and University Hospital, Heinrich-Heine-University Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany.
Carsten HagenbeckClinic for Gynecology and Obstetrics, Medical Faculty, Heinrich-Heine University Düsseldorf, 40225, Düsseldorf, Germany.
Majeed RanaDepartment of Oral-, Maxillofacial and Facial Plastic Surgery, University Hospital Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany.
Jan Frederick CorneliusDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany.
Sajjad MuhammadDepartment of Neurosurgery, Medical Faculty, University Hospital Düsseldorf, Heinrich-Heine- Universität Düsseldorf, Moorenstrasse 5, 40225, Düsseldorf, Germany.
Heinrich Heine University Düsseldorf · DEDüsseldorf University Hospital · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmoking, alcohol abuse, and hypertension are - among others, potential risk factors for cardiovascular diseases. These risk factors generate oxidative stress and cause oxidative stress-induced DNA damage, resulting in cellular senescence and senescence-associated secretory phenotype (SASP). The SASP factors in feed-forward response exacerbate inflammation and cause tissue remodeling, resulting in atherosclerotic plaque formation and rupture.

resultsColchicine inhibited ROS generation and mitigated oxidative stress-induced DNA damage. It dampened oxidative stress-induced endothelial cell senescence and improved the expression of DNA repair protein KU80 and aging marker Lamin B1. The drug attenuated the expression of senescence marker P21 at mRNA and protein levels. The pathway analysis showed that colchicine inhibited NF-κB and MAPKs pathways and subdued mTOR activation. Colchicine also attenuated mRNA expression of interleukin (IL)-1β, IL-6, IL-8, MCP-1, ICAM-1, and E-selectin. Furthermore, colchicine reduced the mRNA and protein expression of matrix metalloproteinase (MMP-2).

conclusionIn summary, colchicine blocked oxidative stress-induced senescence and SASP by inhibiting the activation of NF-κB and MAPKs pathways.

Indexed as

Cellular senescenceColchicineEndothelial cellsInflammationMAPKsmTORNFκ-BOxidative stress

Identifiers

PMID38001470
PMCPMC10675905
OpenAlexW4388969158

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.