Evidence map›Paper›PMID 31013638›Full record

ReviewMolecules (Basel, Switzerland)2019

Oxidative Stress: A Key Modulator in Neurodegenerative Diseases.

Anju Singh, Ritushree Kukreti, Luciano Saso, Shrikant Kukreti

Open access · goldAbstract readReview
In one paragraph

Review in Molecules (Basel, Switzerland), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,100 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
1,100citing papers in PubMed, 3 pooled it
106.9field-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

1,100 citing papers in PubMed, 3 syntheses or guidelines pooled it, 2,145 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Trial
  5. Article
  6. Article
  7. Update on the Physiopathology of Keratoconus.Medical sciences (Basel, Switzerland) · 2026
    Review
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  20. LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026
    Review

1,040 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

4 authors at 3 institutions in 2 countries.

Anju SinghNucleic Acids Research Lab, Department of Chemistry, University of Delhi (North Campus), Delhi 110007, India. anju11278@gmail.com.ORCID 0000-0003-4980-0669
Ritushree KukretiAcademy of Scientific and Innovative Research (AcSIR), CSIR-Institute of Genomics and Integrative Biology (CSIR-IGIB) Campus, Delhi 110007, India. ritus@igib.res.in.
Luciano SasoDepartment of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, P. le Aldo Moro 5, 00185 Rome, Italy. luciano.saso@uniroma1.it.ORCID 0000-0003-4530-8706
Shrikant KukretiNucleic Acids Research Lab, Department of Chemistry, University of Delhi (North Campus), Delhi 110007, India. shrikant.kukreti6@gmail.com.
University of Delhi · INInstitute of Genomics and Integrative Biology · INSapienza University of Rome · IT

Funding

DU/DST PURSE and R&D CD/2016/1761, RC/2015/9677-882
6 · The paper itself

Abstract

Oxidative stress is proposed as a regulatory element in ageing and various neurological disorders. The excess of oxidants causes a reduction of antioxidants, which in turn produce an oxidation-reduction imbalance in organisms. Paucity of the antioxidant system generates oxidative-stress, characterized by elevated levels of reactive species (oxygen, hydroxyl free radical, and so on). Mitochondria play a key role in ATP supply to cells via oxidative phosphorylation, as well as synthesis of essential biological molecules. Various redox reactions catalyzed by enzymes take place in the oxidative phosphorylation process. An inefficient oxidative phosphorylation may generate reactive oxygen species (ROS), leading to mitochondrial dysfunction. Mitochondrial redox metabolism, phospholipid metabolism, and proteolytic pathways are found to be the major and potential source of free radicals. A lower concentration of ROS is essential for normal cellular signaling, whereas the higher concentration and long-time exposure of ROS cause damage to cellular macromolecules such as DNA, lipids and proteins, ultimately resulting in necrosis and apoptotic cell death. Normal and proper functioning of the central nervous system (CNS) is entirely dependent on the chemical integrity of brain. It is well established that the brain consumes a large amount of oxygen and is highly rich in lipid content, becoming prone to oxidative stress. A high consumption of oxygen leads to excessive production of ROS. Apart from this, the neuronal membranes are found to be rich in polyunsaturated fatty acids, which are highly susceptible to ROS. Various neurodegenerative diseases such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and amyotrophic lateral sclerosis (ALS), among others, can be the result of biochemical alteration (due to oxidative stress) in bimolecular components. There is a need to understand the processes and role of oxidative stress in neurodegenerative diseases. This review is an effort towards improving our understanding of the pivotal role played by OS in neurodegenerative disorders.

Indexed as

Oxidative StressAnimalsHumansMitochondriaNeurodegenerative DiseasesOxidation-ReductionReactive Oxygen SpeciesReactive Oxygen SpeciesAlzheimer’s disease (AD)mitochondrianeurodegenerative diseaseoxidative stress (OS)Parkinson’s disease (PD)reactive oxygen species (ROS)

Identifiers

PMID31013638
PMCPMC6514564
OpenAlexW2937074474

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.