Evidence map›Paper›PMID 32312955›Full record

ArticleCell death & disease2020

MSCs ameliorate hepatocellular apoptosis mediated by PINK1-dependent mitophagy in liver ischemia/reperfusion injury through AMPKα activation.

Jun Zheng, Liang Chen, Tongyu Lu, Yingcai Zhang, Xin Sui, Yang Li, Xuna Huang, Liying He, Jianye Cai, Chaorong Zhou and 4 more

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06740149 (Efficacy and Safety of Allogeneic Human Bone Marrow Mesenchymal Stem Cells for the Treatment of Patients With Acute-on-chronic Liver Failure), which is not on this map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 1% 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.

NCT06740149 phase1 / phase2completednot on this mapstarted 2023, after this paper: background citation

Efficacy and Safety of Allogeneic Human Bone Marrow Mesenchymal Stem Cells for the Treatment of Patients With Acute-on-chronic Liver Failure

TypeinterventionalSponsorSun Yat-sen UniversityRan2023 to 2026Enrolled90ConditionsAcute-On-Chronic Liver FailureArmsBone marrow mesenchymal stem cells (low dose), Solvent of CG-BM1, Bone marrow mesenchymal stem cells (medium dose), Bone marrow mesenchymal stem cells (high dose)
3 · Its place in the literature

Who cites it

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.

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  6. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
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5 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 1 country.

Jun Zheng *Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Liang Chen *Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Tongyu Lu *Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Yingcai Zhang *Department of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Xin SuiSurgical Intensive Care Unit, The Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Yang LiDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Xuna HuangCentral Experimental Room of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Liying HeDepartment of Gastroenterology, Guangzhou Women and Children's Medical Center, 510630, Guangzhou, China.
Jianye CaiDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Chaorong ZhouDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Jinliang LiangGuangdong Key Laboratory of Liver Disease Research, Key Laboratory of Liver Disease Biotherapy and Translational Medicine of Guangdong Higher Education Institutes, The Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China.
Guihua ChenDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China. chgh1955@263.net.
Jia YaoDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China. yaojia6@mail.sysu.edu.cn.
Yang YangDepartment of Hepatic Surgery and Liver Transplantation Center of the Third Affiliated Hospital of Sun Yat-sen University, 510630, Guangzhou, China. yysysu@163.com.
Third Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CNGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte apoptosis is the main pathophysiological process underlying liver ischemia/reperfusion (I/R) injury. Mitochondrial abnormalities have a vital role in hepatocellular damage. The hepatoprotective effects of mesenchymal stem cells (MSCs) have been previously demonstrated. In this study, we aim to investigate the effect and potential mechanism of MSCs against liver I/R injury. Effects of MSCs were studied in mice liver I/R injury model and in a hypoxia/reoxygenation (H/R) model of L02 hepatocytes. The potential mechanisms of MSCs on these in vivo and in vitro I/R-induced hepatocellular apoptosis models were studies. Accompanied by the improvement of hepatic damage, MSCs exhibited capabilities of controlling mitochondrial quality, shown by reduced mitochondrial reactive oxygen species (mtROS) overproduction, decreased the accumulation of mitochondrial fragmentation, restored ATP generation and upregulated mitophagy. Furthermore, we descripted a potential mechanism of MSCs on upregulating mitophagy and found that the reduced Parkin and PINK1 expression and inactivated AMPKα pathway were observed in the liver tissue in I/R model. These effects were reversed by MSCs treatment. In vitro study showed that MSC-conditioned medium (MSC-CM) suppressed hepatocellular apoptosis and inhibited mtROS accumulation in the H/R environment. And these effects of MSC-CM were partially blocked after the cells were transfected with PINK1 siRNA or added with dorsomorphin. Collectively, our findings provide a novel pharmacological mechanism that MSCs exert hepatoprotective effect in liver I/R injury via upregulating PINK1-dependent mitophagy. In addition, this effect might be attributed to the modulation of AMPKα activation.

Indexed as

AnimalsApoptosisCarcinoma, HepatocellularCulture Media, ConditionedHepatocytesIschemiaLiver NeoplasmsMaleMesenchymal Stem CellsMice, Inbred C57BLMitochondriaMitophagyReactive Oxygen SpeciesReperfusion InjuryCulture Media, ConditionedReactive Oxygen Species

Identifiers

PMID32312955
PMCPMC7171190
OpenAlexW3016816483

What OpenQuestion holds

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Registered trials

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.