Evidence map›Paper›PMID 35093121›Full record

ReviewBehavioral and brain functions : BBF2022

The interplay between oxidative stress and autophagy: focus on the development of neurological diseases.

Marjan Talebi, Seyyed Ali Mohammadi Vadoud, Alireza Haratian, Mohsen Talebi, Tahereh Farkhondeh, Ali Mohammad Pourbagher-Shahri, Saeed Samarghandian

Abstract readReview
In one paragraph

Review in Behavioral and brain functions : BBF, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

35 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Therapeutic effects ofIBRO neuroscience reports · 2025
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. p66shc deficiency attenuates high glucose-induced autophagy dysfunction in Schwann cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    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

7 authors.

Marjan TalebiDepartment of Pharmacognosy, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Seyyed Ali Mohammadi VadoudDepartment of Pharmaceutical Biotechnology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Alireza HaratianDepartment of Pharmacognosy, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohsen TalebiDepartment of Chemistry and Biochemistry, University of Texas at Arlington, Arlington, TX, 76019, USA.
Tahereh FarkhondehMedical Toxicology and Drug Abuse Research Center (MTDRC), Birjand University of Medical Sciences, Birjand, Iran.
Ali Mohammad Pourbagher-ShahriMedical Toxicology and Drug Abuse Research Center (MTDRC), Birjand University of Medical Sciences, Birjand, Iran.
Saeed SamarghandianNoncommunicable Diseases Research Center, Neyshabur University of Medical Sciences, Neyshabur, Iran. samarghandians1@nums.ac.ir.ORCID http://orcid.org/0000-0001-5461-9579

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regarding the epidemiological studies, neurological dysfunctions caused by cerebral ischemia or neurodegenerative diseases (NDDs) have been considered a pointed matter. Mount-up shreds of evidence support that both autophagy and reactive oxygen species (ROS) are involved in the commencement and progression of neurological diseases. Remarkably, oxidative stress prompted by an increase of ROS threatens cerebral integrity and improves the severity of other pathogenic agents such as mitochondrial damage in neuronal disturbances. Autophagy is anticipated as a cellular defending mode to combat cytotoxic substances and damage. The recent document proposes that the interrelation of autophagy and ROS creates a crucial function in controlling neuronal homeostasis. This review aims to overview the cross-talk among autophagy and oxidative stress and its molecular mechanisms in various neurological diseases to prepare new perceptions into a new treatment for neurological disorders. Furthermore, natural/synthetic agents entailed in modulation/regulation of this ambitious cross-talk are described.

Indexed as

Neurodegenerative DiseasesOxidative StressAutophagyHomeostasisHumansReactive Oxygen SpeciesReactive Oxygen SpeciesAutophagyNeurodegenerative diseasesNeurological diseasesOxidative stressSignaling pathways, Alzheimer’s disease, Parkinson’s disease, Reactive Oxygen Species (ROS)

Identifiers

PMID35093121
PMCPMC8799983

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.