Evidence map›Paper›PMID 39484669›Full record

ReviewNeuroSci2022

Reactive Oxygen Species: Angels and Demons in the Life of a Neuron.

Kasturi Biswas, Kellianne Alexander, Michael M Francis

Abstract readReview
In one paragraph

Review in NeuroSci, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
–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

40 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Mercury-induced excitotoxicity in autism spectrum disorder: disruption of glutamatergic homeostasis and the therapeutic role of the selenium-glutathione axis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
  7. Review
  8. Preclinical Evaluation ofMolecules (Basel, Switzerland) · 2026
    Article
  9. Review
  10. Article
  11. Aging, frailty, and their effects on motor performance: evidence from kinematic analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Article
  12. Combined targeting of PRDX6 and GSTP1 as a potential differentiation strategy for neuroblastoma treatment.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  13. Review
  14. Article
  15. Role of Mitochondrial Dysfunction in Neuropathy.International journal of molecular sciences · 2025
    Review
  16. Article
  17. Article
  18. Memory with a little HNature metabolism · 2025
    Article
  19. Review
  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.

Kasturi BiswasDepartment of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.).ORCID https://orcid.org/0000-0001-7243-1422
Kellianne AlexanderDepartment of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.).ORCID https://orcid.org/0000-0002-4572-2600
Michael M FrancisDepartment of Neurobiology, University of Massachusetts Chan Medical School, Worcester, MA 01605, USA; kasturi.biswas@umassmed.edu (K.B.); kellianne.alexander@umassmed.edu (K.A.).ORCID https://orcid.org/0000-0002-8076-6668

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reactive oxygen species (ROS) have emerged as regulators of key processes supporting neuronal growth, function, and plasticity across lifespan. At normal physiological levels, ROS perform important roles as secondary messengers in diverse molecular processes such as regulating neuronal differentiation, polarization, synapse maturation, and neurotransmission. In contrast, high levels of ROS are toxic and can ultimately lead to cell death. Excitable cells, such as neurons, often require high levels of metabolic activity to perform their functions. As a consequence, these cells are more likely to produce high levels of ROS, potentially enhancing their susceptibility to oxidative damage. In addition, because neurons are generally post-mitotic, they may be subject to accumulating oxidative damage. Thus, maintaining tight control over ROS concentration in the nervous system is essential for proper neuronal development and function. We are developing a more complete understanding of the cellular and molecular mechanisms for control of ROS in these processes. This review focuses on ROS regulation of the developmental and functional properties of neurons, highlighting recent in vivo studies. We also discuss the current evidence linking oxidative damage to pathological conditions associated with neurodevelopmental and neurodegenerative disorders.

Indexed as

brain injuryC. elegansneurodegenerative diseaseneurodevelopmentoxidative stresssynapse

Identifiers

PMID39484669
PMCPMC11523706

What Socratic 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 Socratic graph.