Evidence map›Paper›PMID 30881598›Full record

ArticleOxidative medicine and cellular longevity2019

Coenzyme Q10 Ameliorates Pancreatic Fibrosis via the ROS-Triggered mTOR Signaling Pathway.

Ran Xue, Jianxin Wang, Lixin Yang, Xinjuan Liu, Yan Gao, Yanhua Pang, Yanbin Wang, Jianyu Hao

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  11. Nutraceuticals as Modulators of Autophagy: Relevance in Parkinson's Disease.International journal of molecular sciences · 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 1 institution in 1 country.

Ran XueDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0003-3978-6066
Jianxin WangDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Lixin YangDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Xinjuan LiuDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0001-5817-6699
Yan GaoDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Yanhua PangDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.
Yanbin WangDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0002-4331-3192
Jianyu HaoDepartment of Gastroenterology, Beijing Chao-Yang Hospital, Capital Medical University, Beijing 100020, China.ORCID 0000-0001-7881-9380
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimPancreatic stellate cells (PSCs) play a pivotal role in pancreatic fibrosis. Any remedies that inhibit the activation of PSCs can be potential candidates for therapeutic strategies in pancreatic fibrosis-related pancreatic ductal adenocarcinoma (PDAC) and chronic pancreatitis (CP). Our study is aimed at exploring the protective effect of coenzyme Q10 (CoQ10) against pancreatic fibrosis.

methodsPancreatic fibrosis was induced by 20% L-arginine (250 mg/100 g) at 1 h intervals twice per week for 8 weeks in C57BL/6 mice. CoQ10 was administered for 4 weeks. Isolated primary PSCs from C57BL/6 mice were treated with 100

resultsPretreatment and posttreatment of CoQ10 decreased autophagy, activation of PSCs, oxidative stress, histological changes, and collagen deposition in the CP mouse model. In primary PSCs, expression levels of p-PI3K, p-AKT, and p-mTOR were upregulated with CoQ10. A rescue experiment using specific inhibitors of the PI3K-AKT-mTOR pathway demonstrated that the PI3K-AKT-mTOR signaling pathway was the underlying mechanism by which CoQ10 ameliorated fibrosis. With the addition of Rosup, expression levels of the autophagy biomarkers LC3 and Atg5 were elevated. Meanwhile, the levels of p-PI3K, p-AKT, and p-mTOR were lower.

conclusionsOur findings demonstrated that CoQ10 alleviates pancreatic fibrosis by the ROS-triggered PI3K/AKT/mTOR signaling pathway. CoQ10 may be a therapeutic candidate for antifibrotic methods.

Indexed as

AnimalsFibrosisHumansMaleMiceMice, Inbred C57BLPancreatic NeoplasmsReactive Oxygen SpeciesTOR Serine-Threonine KinasesUbiquinonecoenzyme Q10MTOR protein, humanReactive Oxygen SpeciesTOR Serine-Threonine KinasesUbiquinone

Identifiers

PMID30881598
PMCPMC6383547
OpenAlexW2911662779

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.