Evidence map›Paper›PMID 29052145›Full record

ReviewMolecular neurobiology2018

Cell Death Pathways: a Novel Therapeutic Approach for Neuroscientists.

G Morris, A J Walker, M Berk, M Maes, B K Puri

Abstract readReview
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers.

0numbers the graph read from it
0cells of the map it votes in
85citing 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

85 citing papers in PubMed.

  1. AdjunctiveCanadian journal of psychiatry. Revue canadienne de psychiatrie · 2021
    Trial
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Oxidative Stress in Fetuses and Newborns.Antioxidants (Basel, Switzerland) · 2024
    Article
  12. Review
  13. Article
  14. Review
  15. Curcumin coating: a novel solution to mitigate inherent carbon nanotube toxicity.Journal of materials science. Materials in medicine · 2024
    Article
  16. Review
  17. Review
  18. Stanniocalcin-1 Promotes PARP1-Dependent Cell Death via JNK Activation in Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  19. Review
  20. Article

25 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

5 authors.

G Morris, Bryn Road Seaside 87, Llanelli, Wales, , SA15 2LW, UK.
A J WalkerSchool of Medicine, Deakin University, Geelong, 3220, Australia.
M BerkThe Centre for Molecular and Medical Research, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia.
M MaesSchool of Medicine, Deakin University, Geelong, 3220, Australia.
B K PuriDepartment of Medicine, Hammersmith Hospital, Imperial College London, London, W12 0HS, UK. basant.puri@imperial.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the first part, the following mechanisms involved in different forms of cell death are considered, with a view to identifying potential therapeutic targets: tumour necrosis factor receptors (TNFRs) and their engagement by tumour necrosis factor-alpha (TNF-α); poly [ADP-ribose] polymerase (PARP)-1 cleavage; the apoptosis signalling kinase (ASK)-c-Jun N-terminal kinase (JNK) axis; lysosomal permeability; activation of programmed necrotic cell death; oxidative stress, caspase-3 inhibition and parthanatos; activation of inflammasomes by reactive oxygen species and the development of pyroptosis; oxidative stress, calcium dyshomeostasis and iron in the development of lysosomal-mediated necrosis and lysosomal membrane permeability; and oxidative stress, lipid peroxidation, iron dyshomeostasis and ferroptosis. In the second part, there is a consideration of the role of lethal and sub-lethal activation of these pathways in the pathogenesis and pathophysiology of neurodegenerative and neuroprogressive disorders, with particular reference to the TNF-α-TNFR signalling axis; dysregulation of ASK-1-JNK signalling; prolonged or chronic PARP-1 activation; the role of pyroptosis and chronic inflammasome activation; and the roles of lysosomal permeabilisation, necroptosis and ferroptosis. Finally, it is suggested that, in addition to targeting oxidative stress and inflammatory processes generally, neuropsychiatric disorders may respond to therapeutic targeting of TNF-α, PARP-1, the Nod-like receptor NLRP3 inflammasome and the necrosomal molecular switch receptor-interacting protein kinase-3, since their widespread activation can drive and/or exacerbate peripheral inflammation and neuroinflammation even in the absence of cell death. To this end, the use is proposed of a combination of the tetracycline derivative minocycline and N-acetylcysteine as adjunctive treatment for a range of neuropsychiatric disorders.

Indexed as

ApoptosisMolecular Targeted TherapyNeurosciencesAnimalsHumansNervous System DiseasesReactive Oxygen SpeciesTumor Necrosis Factor-alphaReactive Oxygen SpeciesTumor Necrosis Factor-alphaApoptosisFerroptosisMinocyclineN-acetylcysteineNecroptosisNeuropsychiatric disorders

Identifiers

PMID29052145
PMCPMC5994217

What OpenQuestion holds

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Registered trials

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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.