Evidence map›Paper›PMID 38097957›Full record

ArticleBMC pulmonary medicine2023

Cellular senescence contributes to mechanical ventilation-induced diaphragm dysfunction by upregulating p53 signalling pathways.

Weimin Shen, Ye Jiang, Ying Xu, Xiaoli Qian, Jianwei Jia, Yuejia Ding, Yuhan He, Qing Pan, Jinyang Zhuang, Huiqing Ge and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC pulmonary medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
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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

11 authors at 4 institutions in 1 country.

Weimin Shen *Department of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Ye Jiang *Department of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Ying Xu *Department of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Xiaoli QianDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Jianwei JiaDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Yuejia DingDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Yuhan HeDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China.
Qing PanCollege of Information Engineering, Zhejiang University of Technology, Hangzhou, 310023, China.
Jinyang ZhuangHuashan Hospital affiliated to Fudan University, Shanghai, 200040, China.
Huiqing GeDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China. gehq@zju.edu.cn.
Peifeng XuDepartment of Respiratory Care, Regional Medical Center for National Institute of Respiratory Diseases, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Qingchun East Rd. 3, Hangzhou, 310016, China. 3408168@zju.edu.cn.
Sir Run Run Shaw Hospital · CNZhejiang University · CNFudan University · CNZhejiang University of Technology · CN

Funding

National Natural Science Foundation of China 82070087Natural Science Foundation of Zhejiang Province GD22H019093
6 · The paper itself

Abstract

backgroundMechanical ventilation can cause acute atrophy and injury in the diaphragm, which are related to adverse clinical results. However, the underlying mechanisms of ventilation-induced diaphragm dysfunction (VIDD) have not been well elucidated. The current study aimed to explore the role of cellular senescence in VIDD.

methodsA total of twelve New Zealand rabbits were randomly divided into 2 groups: (1) spontaneously breathing anaesthetized animals (the CON group) and (2) mechanically ventilated animals (for 48 h) in V-ACV mode (the MV group). Respiratory parameters were collected during ventilation. Diaphragm were collected for further analyses.

resultsCompared to those in the CON group, the percentage and density of sarcomere disruption in the MV group were much higher (p < 0.001, both). The mRNA expression of MAFbx and MuRF1 was upregulated in the MV group (p = 0.003 and p = 0.006, respectively). Compared to that in the CON group, the expression of MAFbx and MuRF1 detected by western blotting was also upregulated (p = 0.02 and p = 0.03, respectively). Moreover, RNA-seq showed that genes associated with senescence were remarkably enriched in the MV group. The mRNA expression of related genes was further verified by q-PCR (Pai1: p = 0.009; MMP9: p = 0.008). Transverse cross-sections of diaphragm myofibrils in the MV group showed more intensive positive staining of SA-βGal than those in the CON group. p53-p21 axis signalling was elevated in the MV group. The mRNA expression of p53 and p21 was significantly upregulated (p = 0.02 and p = 0.05, respectively). The western blot results also showed upregulation of p53 and p21 protein expression (p = 0.03 and p = 0.05, respectively). Moreover, the p21-positive staining in immunofluorescence and immunohistochemistry in the MV group was much more intense than that in the CON group (p < 0.001, both).

conclusionsIn a rabbit model, we demonstrated that mechanical ventilation in A/C mode for 48 h can still significantly induce ultrastructural damage and atrophy of the diaphragm. Moreover, p53-dependent senescence might play a role in mechanical ventilation-induced dysfunction. These findings might provide novel therapeutic targets for VIDD.

Indexed as

DiaphragmRespiration, ArtificialAnimalsAtrophyCellular SenescenceRabbitsRNA, MessengerTumor Suppressor Protein p53RNA, MessengerTumor Suppressor Protein p53Cellular senescenceDiaphragm dysfunctionMechanical ventilationp53-p21 axis

Identifiers

PMID38097957
PMCPMC10722656
OpenAlexW4389725592

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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.