Evidence map›Paper›PMID 36419003›Full record

ArticleBMC pulmonary medicine2022

Circadian clock gene Clock-Bmal1 regulates cellular senescence in Chronic obstructive pulmonary disease.

Lingling Li, Min Zhang, Chunyang Zhao, Yusheng Cheng, Chuanmei Liu, Minhua Shi

Open access · goldAbstract read
In one paragraph

Article in BMC pulmonary medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
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  7. Parenchymal and inflammatory responses to ozone exposure in the aging healthy and surfactant protein C mutant lung.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  8. Article
  9. Peripheral clocks and systemicFrontiers in endocrinology · 2025
    Review
  10. Article
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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

6 authors at 3 institutions in 1 country.

Lingling LiDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Min ZhangDepartment of Emergency, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Chunyang ZhaoDepartment of Pulmonary and Critical Care Medicine, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Yusheng ChengDepartment of Pulmonary and Critical Care Medicine, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Chuanmei LiuDepartment of Pulmonary and Critical Care Medicine, Yijishan Hospital, Wannan Medical College, Wuhu, China.
Minhua ShiDepartment of Pulmonary and Critical Care Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, China. Shiminhua@163.com.
First Affiliated Hospital of Wannan Medical College · CNSoochow University · CNWannan Medical College · CN

Funding

Anhui Provincial Key projects of Natural Science Foundation for Colleges and Universities KJ2021A0834Key projects of Wannan Medical College WK2021ZF11
6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a progressive respiratory disease. COPD is associated with accelerated lung aging. Circadian clock is believed to play important roles in COPD. Although the circadian molecular clock regulates cellular senescence, there is no information available regarding the impact of COPD. The aim of this study is to investigate the role of the circadian clock protein BMAL1 and CLOCK in cellular senescence in order to understand the cellular mechanisms of accelerated aging of COPD. Bmal1 and Clock levels were assessed in the plasma samples of non-smokers, smokers, and patients with COPD. The regulation of ciracadian clock expression and cell senescence by cigarette smoke extract (CSE) was studied in vitro, and small interfering RNA (siRNA) and overexpression of Bmal1 or Clock were employed to investigate the role of circadian clock on cell senescence. Herein, patients with COPD showed lower Bmal1 and Clock expression in the plasma. Interestingly, CSE exposure contributed to the increased cell senescence, decreased Clock and Bmal1 in human bronchial epithelial cells (Beas-2B cells). We found that knockdown of Clock or Bmal1 lead to upregulation of cell senescence in Beas-2B cells, while overexpression of Clock or Bmal1 inhibited cell senescence in Beas-2B cells, which is through the MAPK pathways. Therefore, our findings indicated that Bmal1 or Clock deficiency may be a significant factor to increase cellular senescence of the lung to develop COPD.

Indexed as

Circadian ClocksPulmonary Disease, Chronic ObstructiveAgingARNTL Transcription FactorsCellular SenescenceHumansARNTL Transcription FactorsChronic obstructive Pulmonary Disease (COPD)Circadian clockSenescenceSmoke

Identifiers

PMID36419003
PMCPMC9682805
OpenAlexW4309713191

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.