Evidence map›Paper›PMID 28889229›Full record

ArticleCell stress & chaperones2018

Melatonin alleviates inflammation-induced apoptosis in human umbilical vein endothelial cells via suppression of Ca

Jiasen Cui, Zeng Li, Shunjiu Zhuang, Shaohong Qi, Li Li, Junwen Zhou, Wan Zhang, Yun Zhao

Open access · greenAbstract read
In one paragraph

Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

33 citing papers in PubMed, 63 citations in OpenAlex.

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  15. Mitochondria signaling pathways in allergic asthma.Journal of investigative medicine : the official publication of the American Federation for Clinical Research · 2022
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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.

Jiasen CuiDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China. guanj301@163.com.
Zeng LiDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Shunjiu ZhuangDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Shaohong QiDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Li LiDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Junwen ZhouDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Wan ZhangDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Yun ZhaoDepartment of Vascular Surgery, Huadong Hospital, Fudan University, Shanghai, 200040, China.
Fudan University · CNHuadong Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelia inflammation damage is vital to the development and progression of chronic venous disease. In the present study, we explored the protective effect of melatonin on endothelia apoptosis induced by LPS, particularly focusing on the mitochondrial fission. We demonstrated that human umbilical vein endothelial cells (HUVEC) subjected to LPS for 12 h exhibited a higher apoptotic rate. However, melatonin (1-20 μM) treatment 12 h before LPS had the ability to protect HUVEC cell against LPS-mediated apoptosis in a dose-dependent manner. Furthermore, LPS induced the cytoplasmic calcium overload which was responsible for the upregulation of calcium-dependent xanthine oxidase (XO). Higher XO expression was associated with reactive oxygen species (ROS) overproduction, leading to the Drp1 phosphorylation at the Ser616 site and migration on the surface of mitochondria. Furthermore, phosphorylated Drp1 initiated the mitochondrial fission contributing to the caspase9-dependent mitochondrial apoptosis as evidenced by lower membrane potential, more cyt-c leakage into the nuclear, and higher expression of proapoptotic proteins. However, melatonin treatment could trigger the AMPK pathway, which was followed by the increased SERCA2a expression. Activation of AMPK/SERCA2a by melatonin inhibited the calcium overload, XO-mediated ROS outburst, Drp1-required mitochondrial fission, and final mitochondrial apoptosis. In summary, this study confirmed that LPS induced HUVEC apoptosis through Ca

Indexed as

Signal TransductionAdenylate KinaseApoptosisCalciumCaspase 9HumansHuman Umbilical Vein Endothelial CellsInflammationLipopolysaccharidesMelatoninMitochondriaMitochondrial DynamicsReactive Oxygen SpeciesSarcoplasmic Reticulum Calcium-Transporting ATPasesUp-RegulationXanthine OxidaseAdenylate KinaseCalciumCaspase 9LipopolysaccharidesMelatoninReactive Oxygen SpeciesSarcoplasmic Reticulum Calcium-Transporting ATPasesXanthine OxidaseAMPKCalcium overloadHUVECLPSMelatoninMitochondrial fissionOxidative stressSERCA2a

Identifiers

PMID28889229
PMCPMC5823809
OpenAlexW2755416799

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.