Evidence map›Paper›PMID 36928143›Full record

ArticleLung2023

Melatonin Protects Against Hyperoxia-Induced Apoptosis in Alveolar Epithelial type II Cells by Activating the MT2/PI3K/AKT/ETS1 Signaling Pathway.

Fan He, Qiao-Fang Wang, Lin Li, Cong Yu, Chun-Zi Liu, Wen-Chao Wei, Li-Ping Chen, Huan-Yu Li

Abstract read
PubMed Publisher
In one paragraph

Article in Lung, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Melatonin in lung cancer: integrating molecular mechanisms, tumor microenvironment regulation, apoptotic signaling, and therapeutic opportunities.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026
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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 2 institutions in 1 country.

Fan HeDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Qiao-Fang WangDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Lin LiDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Cong YuDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Chun-Zi LiuDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Wen-Chao WeiDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China.
Li-Ping ChenDepartment of Neonatology, Jiangxi Provincial Children's Hospital, No. 1666, DieziHu Road, Honggutan District, Nanchang, 330038, Jiangxi, China. ccllpp88@qq.com.ORCID 0000-0002-3704-2808
Huan-Yu LiSecond Department of Respiratory Disease, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, No. 152, Aiguo Road, DongHu District, Nanchang, 330006, Jiangxi, China. huanyu15270882512@163.com.ORCID 0000-0003-4196-4490
Jiangxi Provincial Children's Hospital · CNFirst Affiliated Hospital of Jiangxi Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeHyperoxia-induced apoptosis in alveolar epithelial type II cells (AECIIs) plays a critical role in the development of bronchopulmonary dysplasia (BPD). Melatonin has been shown to improve BPD. However, the protective effect of melatonin on hyperoxia-induced apoptosis in AECIIs and the precise mechanisms involved remain unclear.

methodsHuman alveolar epithelial type II A549 cells were treated with hyperoxia as an in vitro model to investigate the antiapoptotic mechanism of melatonin. CCK-8 assays were performed to investigate the viability of A549 cells. Hoechst 33,258 staining was carried out to quantify apoptosis in A549 cells. The protein expression levels of E26 oncogene homolog 1 (ETS1), Bcl-2, Bax, Bim, Wnt, β-catenin, AKT and phosphorylated AKT were measured by western blotting. LY294002, SC79 and the downregulation of ETS1, melatonin receptor 1 (MT1) and MT2 with specific siRNAs were used to investigate the role of the PI3K/AKT pathway, ETS1, MT1 and MT2 in hyperoxia-induced apoptosis in A549 cells.

resultsMelatonin prevented hyperoxia-induced apoptosis in A549 cells, and the upregulation of E26 oncogene homolog 1 (ETS1) contributed to the antiapoptotic effect of melatonin. Melatonin activated the PI3K/AKT axis, which led to ETS1 upregulation and inhibited apoptosis in hyperoxia-exposed A549 cells. Furthermore, melatonin-induced activation of the PI3K/AKT axis, upregulation of ETS1 and inhibition of apoptosis were reversed by melatonin receptor 2 (MT2) siRNA in hyperoxia-exposed A549 cells.

conclusionMelatonin prevents hyperoxia-induced apoptosis by activating the MT2/PI3K/AKT/ETS1 axis in alveolar epithelial cells.

Indexed as

Bronchopulmonary DysplasiaHyperoxiaMelatoninAlveolar Epithelial CellsApoptosisEpithelial CellsHumansInfant, NewbornPhosphatidylinositol 3-KinasesProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-aktReceptors, MelatoninSignal TransductionETS1 protein, humanMelatoninPhosphatidylinositol 3-KinasesProto-Oncogene Protein c-ets-1Proto-Oncogene Proteins c-aktReceptors, MelatoninApoptosisBronchopulmonary dysplasiaETS1Lung injuryMelatoninMelatonin receptors

Identifiers

PMID36928143
OpenAlexW4327684932

What OpenQuestion holds

Textmetadata
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.