Evidence map›Paper›PMID 38299199›Full record

ReviewGenes & diseases2024

Mitochondrial dysfunction: A promising therapeutic target for liver diseases.

Ping Chen, Lichao Yao, Mengqin Yuan, Zheng Wang, Qiuling Zhang, Yingan Jiang, Lanjuan Li

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
12.9field-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.

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

69 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  8. Genetic ablation ofiScience · 2026
    Article
  9. Article
  10. Review
  11. Addressing Alcohol Use Disorder in Alcohol-Associated Liver Disease.Clinical and translational gastroenterology · 2026
    Review
  12. Review
  13. Review
  14. Albumin Restores Endothelial Cell Mitochondrial Morphology in Patients With Decompensated Cirrhosis.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

9 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

7 authors at 3 institutions in 1 country.

Ping ChenDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Lichao YaoDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Mengqin YuanDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Zheng WangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Qiuling ZhangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Yingan JiangDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Lanjuan LiDepartment of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, China.
Renmin Hospital of Wuhan University · CNWuhan University · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver is an important metabolic and detoxification organ and hence demands a large amount of energy, which is mainly produced by the mitochondria. Liver tissues of patients with alcohol-related or non-alcohol-related liver diseases contain ultrastructural mitochondrial lesions, mitochondrial DNA damage, disturbed mitochondrial dynamics, and compromised ATP production. Overproduction of mitochondrial reactive oxygen species induces oxidative damage to mitochondrial proteins and mitochondrial DNA, decreases mitochondrial membrane potential, triggers hepatocyte inflammation, and promotes programmed cell death, all of which impair liver function. Mitochondrial DNA may be a potential novel non-invasive biomarker of the risk of progression to liver cirrhosis and hepatocellular carcinoma in patients infected with the hepatitis B virus. We herein present a review of the mechanisms of mitochondrial dysfunction in the development of acute liver injury and chronic liver diseases, such as hepatocellular carcinoma, viral hepatitis, drug-induced liver injury, alcoholic liver disease, and non-alcoholic fatty liver disease. This review also discusses mitochondrion-centric therapies for treating liver diseases.

Indexed as

Chronic diseasesLiver damageMesenchymal stem cellMitochondrialdysfunctionOxidative stress

Identifiers

PMID38299199
PMCPMC10828599
OpenAlexW4386813314

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.