Evidence map›Paper›PMID 29138968›Full record

ArticleMetabolic brain disease2018

Mitochondrial dysfunctions contribute to energy deficits in rodent model of hepatic encephalopathy.

Saurabh Dhanda, Aditya Sunkaria, Avishek Halder, Rajat Sandhir

Abstract read
PubMed Publisher
In one paragraph

Article in Metabolic brain disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Mechanistic insights into the liver-brain axis during chronic liver disease.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Abnormal brain oxygen homeostasis in an animal model of liver disease.JHEP reports : innovation in hepatology · 2022
    Article
  14. Article
  15. The neurogliovascular unit in hepatic encephalopathy.JHEP reports : innovation in hepatology · 2021
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Saurabh DhandaDepartment of Biochemistry, Panjab University, Basic Medical Science Block-II, Sector-25, Chandigarh, 160014, India.
Aditya SunkariaDepartment of Biochemistry, Panjab University, Basic Medical Science Block-II, Sector-25, Chandigarh, 160014, India.
Avishek HalderDepartment of Biochemistry, Panjab University, Basic Medical Science Block-II, Sector-25, Chandigarh, 160014, India.
Rajat SandhirDepartment of Biochemistry, Panjab University, Basic Medical Science Block-II, Sector-25, Chandigarh, 160014, India. sandhir@pu.ac.in.
Panjab University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Perturbations in the cerebral energy metabolism are anticipated to be an important factor by which ammonia may exert its toxic effects on the central nervous system. The present study was designed to investigate the role of impaired mitochondrial functions and cerebral energy metabolism in the development hepatic encephalopathy (HE) induced by of bile duct ligation (BDL). After four weeks of BDL, a significant increase in hepatic hydroxyproline and collagen content was observed which confirmed biliary fibrosis. Brain regions viz. cortex, hippocampus, striatum and cerebellum of BDL rats had impaired activity of mitochondrial respiratory chain enzymes. This was accompanied by increase in mitochondrial reactive oxygen species (ROS), malondialdehyde (MDA) and protein carbonyl levels in the brain. Mitochondrial redox ratio was significantly reduced in the brain of BDL rats. In addition, mitochondria from brain of BDL rats were depolarized and swollen compared to the sham controls. Ultrastructure analysis of mitochondria from cortex and hippocampus of BDL animals revealed aberrant cristae, ruptured membranes and non-dense matrix. Further, a significant decrease was observed in creatine kinase activity, glucose uptake and CO

Indexed as

AnimalsBrainDisease Models, AnimalEnergy MetabolismHepatic EncephalopathyLiverMaleMitochondriaOxidative StressRats, WistarReactive Oxygen SpeciesReactive Oxygen SpeciesAmmoniaBile duct ligationEnergy metabolismHepatic encephalopathyMitochondriaOxidative stress

Identifiers

PMID29138968
OpenAlexW2769967230

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.