Evidence map›Paper›PMID 26135512›Full record

ArticleMolecular medicine reports2015

Promotion of mitochondrial energy metabolism during hepatocyte apoptosis in a rat model of acute liver failure.

Li-Yan Chen, Baoshan Yang, Li Zhou, Feng Ren, Zhong-Ping Duan, Ying-Ji Ma

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Roles of the Keap1/Nrf2 pathway and mitophagy in liver diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  4. Article
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  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Mitochondrial Dysfunction and Chronic Liver Disease.Current issues in molecular biology · 2022
    Review
  14. Article
  15. Antioxidant and Anti-Inflammatory Activity ofAntioxidants (Basel, Switzerland) · 2021
    Article
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article
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

6 authors at 4 institutions in 1 country.

Li-Yan ChenThe Second Department of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Baoshan YangThe Second Department of Infectious Diseases, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150081, P.R. China.
Li ZhouBeijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
Feng RenBeijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
Zhong-Ping DuanBeijing Artificial Liver Treatment and Training Center, Beijing Youan Hospital, Capital Medical University, Beijing 100069, P.R. China.
Ying-Ji MaThe Fourth Department of Infectious Diseases, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150001, P.R. China.
Beijing YouAn Hospital · CNSecond Affiliated Hospital of Harbin Medical University · CNCapital Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatocyte apoptosis and energy metabolism in mitochondria have an important role in the mechanism of acute liver failure (ALF). However, data on the association between apoptosis and the energy metabolism of hepatocytes are lacking. The current study assessed the activity of several key enzymes in mitochondria during ALF, including citrate synthase (CS), carnitine palmitoyltransferase‑1 (CPT‑1) and cytochrome c oxidase (COX), which are involved in hepatocyte energy metabolism. A total of 40 male Sprague‑Dawley rats were divided into five groups and administered D‑galactosamine and lipopolysaccharide to induce ALF. Hepatic pathology and terminal deoxynucleotidyl transferase‑mediated dUTP nick end labeling examinations indicated that hepatocyte apoptosis was observed at 4 h and increased 8 h after ALF. Hepatocyte necrosis appeared at 12 h and was significantly higher at 24 h with inflammatory cell invasion. The results measured by electron microscopy indicated that ultrastructural changes in mitochondria began at 4 h and the mitochondrial outer membrane was completely disrupted at 24 h resulting in mitochondrial collapse. The expression of CS, CPT‑1 and COX was measured and analyzed using assay kits. The activity and protein expression of CS, CPT‑1 and COX began to increase at 4 h, reached a peak at 8 h and decreased at 12 h during ALF. The activities of CS, CPT‑1 and COX were enhanced during hepatocyte apoptosis suggesting that these enzymes are involved in the initiation and development of ALF. Therefore, these results demonstrated that energy metabolism is important in hepatocyte apoptosis during ALF and hepatocyte apoptosis is an active and energy‑consuming procedure. The current study on how hepatocyte energy metabolism affects the transmission of death signals may provide a basis for the early diagnosis and development of an improved therapeutic strategy for ALF.

Indexed as

Alanine TransaminaseAnimalsApoptosisAspartate AminotransferasesBilirubinCarnitine O-PalmitoyltransferaseCitrate (si)-SynthaseElectron Transport Complex IVEnergy MetabolismGalactosamineGene Expression RegulationHepatocytesLipopolysaccharidesLiverLiver Failure, AcuteMaleAlanine TransaminaseAspartate AminotransferasesBilirubinCarnitine O-PalmitoyltransferaseCitrate (si)-SynthaseElectron Transport Complex IVGalactosamineLipopolysaccharides

Identifiers

PMID26135512
PMCPMC4581801
OpenAlexW1936992221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.