Evidence map›Paper›PMID 39588388›Full record

ArticleOpen medicine (Warsaw, Poland)2024

Significant role and the underly mechanism of cullin-1 in chronic obstructive pulmonary disease.

Wenbo Hao, Fei Lin, Weili Kong, Hanbing Shi, Haiying Dong, Zhanjiang Guan, Guohua Liu, Xiao Wang, Li Wang, Moran Liu and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Open medicine (Warsaw, Poland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

11 authors.

Wenbo HaoCardiothoracic Surgery, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Fei LinEndocrinology, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Weili KongDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Hanbing ShiDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Haiying DongPathology and Pathophysiology, Qiqihar Medical University, Qiqihar, 161006, China.
Zhanjiang GuanIntensive Care Unit, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Guohua LiuDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Xiao WangDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Li WangRadiology Imaging Diagnosis Center, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Moran LiuTest Center, The Third Affiliated Hospital of Qiqihar Medical University, Qiqihar, 161006, China.
Yunfei JiangDepartment of Respiratory and Critical Care Medicine, The Third Affiliated Hospital of Qiqihar Medical University, No. 27 Taishun Street, Tiefeng District, Qiqihar, 161006, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study investigated the role and mechanisms of cullin-1 (CUL1) in chronic obstructive pulmonary disease (COPD). Methods: Cigarette smoke extract (CSE)-treated mouse pulmonary microvascular endothelial cells (mPMECs) and cigarette smoke inhalation (CSI)-stimulated mice were used to construct Results: CUL1 expression was downregulated in COPD. CUL1 overexpression significantly promoted cell viability, reduced cell apoptosis, and inhibited inflammatory responses and oxidative stress in CSE-treated mPMECs. These changes were reversed by the p53 agonist nutlin-3. In addition, CUL1 overexpression significantly relieved COPD in mice, as confirmed by the reduced secretion of inflammatory factors in BALF, inhibited oxidative stress response, and improved lung function. Conclusion: CUL1 plays a protective role in CSE-treated mPMECs and CSI-stimulated mice by inhibiting the p53 signaling pathway.

Indexed as

chronic obstructive pulmonary diseasecigarette smoke extractcigarette smoke inhalationcullin-1p53 pathway

Identifiers

PMID39588388
PMCPMC11587924

What Socratic 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 Socratic graph.