Evidence map›Paper›PMID 31692944›Full record

ReviewInternational journal of medical sciences2019

Potential for therapeutic use of hydrogen sulfide in oxidative stress-induced neurodegenerative diseases.

Rubaiya Tabassum, Na Young Jeong

Open access · goldAbstract readReview
In one paragraph

Review in International journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 3 pooled it
8.0field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 3 syntheses or guidelines pooled it, 123 citations in OpenAlex.

  1. Pooled it
  2. Recent Advances in Molecular Research on Hydrogen Sulfide (HInternational journal of molecular sciences · 2022
    Pooled it
  3. Pooled it
  4. Beneficial Effects of Putative Hydrogen Sulfide (HMolecules (Basel, Switzerland) · 2026
    Article
  5. Article
  6. Article
  7. Is Obesity a Modifiable Risk Factor in Multiple Sclerosis? Mechanistic Insights into Neuroinflammation and Oxidative Damage.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Sulfide regulation and catabolism in health and disease.Signal transduction and targeted therapy · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Article

3 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

2 authors at 1 institution in 1 country.

Rubaiya TabassumDepartment of Anatomy and Cell Biology, College of Medicine, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea.
Na Young JeongDepartment of Anatomy and Cell Biology, College of Medicine, Dong-A University, 32, Daesingongwon-ro, Seo-gu, Busan, 49201, Korea.
Dong-A University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative phosphorylation is a source of energy production by which many cells satisfy their energy requirements. Endogenous reactive oxygen species (ROS) are by-products of oxidative phosphorylation. ROS are formed due to the inefficiency of oxidative phosphorylation, and lead to oxidative stress that affects mitochondrial metabolism. Chronic oxidative stress contributes to the onset of neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS). The immediate consequences of oxidative stress include lipid peroxidation, protein oxidation, and mitochondrial deoxyribonucleic acid (mtDNA) mutation, which induce neuronal cell death. Mitochondrial binding of amyloid-β (Aβ) protein has been identified as a contributing factor in AD. In PD and HD, respectively, α-synuclein (α-syn) and huntingtin (Htt) gene mutations have been reported to exacerbate the effects of oxidative stress. Similarly, abnormalities in mitochondrial dynamics and the respiratory chain occur in ALS due to dysregulation of mitochondrial complexes II and IV. However, oxidative stress-induced dysfunctions in neurodegenerative diseases can be mitigated by the antioxidant function of hydrogen sulfide (H

Indexed as

AnimalsAntioxidantsBrainCalcium ChannelsClinical Trials, Phase III as TopicDisease Models, AnimalGlutathioneGlutathione PeroxidaseHumansHydrogen SulfideLipid PeroxidationMitochondriaMitochondrial DynamicsNeurodegenerative DiseasesNeuronsOxidative StressAntioxidantsCalcium ChannelsGlutathioneGlutathione PeroxidaseHydrogen Sulfidemitochondrial K(ATP) channelPotassium ChannelsReactive Oxygen SpeciesSuperoxide Dismutasecentral nervous systemhydrogen sulphidemitochondrial dysfunctionneurodegenerative diseasesoxidative stress

Identifiers

PMID31692944
PMCPMC6818192
OpenAlexW2975469258

What OpenQuestion 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 OpenQuestion graph.