Evidence map›Paper›PMID 33566285›Full record

ReviewBiological trace element research2022

Mitochondrial Dysfunction in Arsenic-Induced Hepatotoxicity: Pathogenic and Therapeutic Implications.

Chandra Prakash, Sunil Chhikara, Vijay Kumar

Abstract readReview
PubMed Publisher
In one paragraph

Review in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
4.8field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Impact of Traditional Chinese Medicine Antioxidants on Oxidative Stress and Drug-Induced Liver Injury: A Review.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Review
  11. Article
  12. Article
  13. Calcitriol Inhibits NaAsOBiological trace element research · 2024
    Article
  14. Review
  15. Review
  16. Arsenic disrupts extracellular vesicle-mediated signaling in regenerating myofibers.Toxicological sciences : an official journal of the Society of Toxicology · 2023
    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

3 authors at 2 institutions in 1 country.

Chandra PrakashNeurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, 110067, India.
Sunil ChhikaraApplied Sciences, UIET, Maharshi Dayanand University, Rohtak, Haryana, 124001, India.
Vijay KumarDepartment of Biochemistry, Maharshi Dayanand University, Rohtak, Haryana, 124001, India. vksiwach.biochem@mdurohtak.ac.in.ORCID http://orcid.org/0000-0001-5559-0624
Maharshi Dayanand University · INJawaharlal Nehru University · IN

Funding

Indian Council of Medical Research 58/51/2011-BMS
6 · The paper itself

Abstract

Mitochondria are vital cellular organelles associated with energy production as well as cell signaling pathways. These organelles, responsible for metabolism, are highly abundant in hepatocytes that make them key players in hepatotoxicity. The literature suggests that mitochondria are targeted by various environmental pollutants. Arsenic, a toxic metalloid known as an environmental pollutant, readily contaminates drinking water and exerts toxic effects. It is toxic to various cellular organs; among them, the liver seems to be most affected. A growing body of evidence suggests that within cells, arsenic is highly toxic to mitochondria and reported to cause oxidative stress and alter an array of signaling pathways and functions. Hence, it is imperative to highlight the mechanisms associated with altered mitochondrial functions and integrity in arsenic-induced liver toxicity. This review provides the details of mechanistic aspects of mitochondrial dysfunction in arsenic-induced hepatotoxicity as well as various ameliorative measures undertaken concerning mitochondrial functions.

Indexed as

ArsenicArsenic PoisoningHumansLiverMitochondriaOxidative StressArsenicArsenicHepatotoxicityLiverMitochondriaOxidative stress

Identifiers

PMID33566285
OpenAlexW3127517073

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.