Evidence map›Paper›PMID 38817823›Full record

ArticleInternational journal of chronic obstructive pulmonary disease2024

A miRNA-21-Mediated PTEN/Akt/NF-κB Axis Promotes Chronic Obstructive Pulmonary Disease Pathogenesis.

Xiaoyan Sai, Chu Qin, Zixiao Zhang, Haoda Yu, Tao Bian

Abstract read
In one paragraph

Article in International journal of chronic obstructive pulmonary disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

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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

5 authors.

Xiaoyan Sai *Department of Respiratory Medicine, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214000, People's Republic of China.ORCID 0000-0002-4201-5353
Chu Qin *Department of Respiratory Medicine, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214000, People's Republic of China.
Zixiao Zhang *Department of Respiratory Medicine, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214000, People's Republic of China.
Haoda YuDepartment of Respiratory Medicine, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214000, People's Republic of China.
Tao BianDepartment of Respiratory Medicine, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214000, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: This study sought to explore the underlying mechanism of miR-21 mediated apoptosis and inflammation in chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS). Methods: We detected levels and PTEN/Akt/NF-κB axis protein levels in peripheral lung tissues of COPD patients and CS-exposed mice and HBE cells. Western blotting assay was used to determine the expression of cleaved caspase-3. IL-6 and IL-8 protein was detected in cell supernatant from cells by ELISA. HBE cells were transfected with a miR-21 inhibitor, and co-culture with A549. Results: Increased miR-21 expression, reduced PTEN expression and following activation of Akt in in peripheral lung tissues of COPD patients and CS-exposed mice and HBE cells. Inhibition of miR-21 showed enhanced PTEN levels and reduced the expression of phosphorylated form of Akt and NF-κB. Decreased expression of cleaved caspase-3, IL-6 and IL-8 in A549 cells co cultured with HBE cells transfected with miR-21 inhibitor compared with transfected with miR-21 control inhibitor. Conclusion: MiR-21 contributes to COPD pathogenesis by modulating apoptosis and inflammation through the PTEN/Akt/NF-κB pathway. Targeting miR-21 may increase PTEN expression and inhibit Akt/NF-κB pathway, offering potential diagnostic and therapeutic value in COPD management.

Indexed as

MicroRNAsNF-kappa BProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePulmonary Disease, Chronic ObstructiveA549 CellsAgedAnimalsApoptosisCigarette SmokingDisease Models, AnimalFemaleHumansInflammation MediatorsInterleukin-6Interleukin-8CXCL8 protein, humanInflammation MediatorsInterleukin-6Interleukin-8MicroRNAsMIRN21 microRNA, humanMIRN21 microRNA, mouseNF-kappa BProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, humanPten protein, mouseapoptosisCOPDinflammationmiR-21PTEN/Akt/NF-κB axis

Identifiers

PMID38817823
PMCPMC11137736

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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 OpenQuestion graph.