Evidence map›Paper›PMID 41498028›Full record

ReviewMediators of inflammation2025

Interplay Between Key Molecular Signaling Pathways and Immune Players Following Brain Irradiation.

Seidu A Richard

Abstract readReview
In one paragraph

Review in Mediators of inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

1 author.

Seidu A RichardDepartment of Biochemistry and Forensic Sciences, School of Chemical and Biochemical Sciences, C. K. Tedam University of Technology and Applied Sciences (CKT-UTAS), P.O. Box 24, Navrongo, Ghana, cktutas.edu.gh.ORCID https://orcid.org/0000-0003-3475-0363

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Irradiation (IRT) has been used extensively for the diagnosis and treatment of primary as well as metastatic brain tumors. Although the susceptibility of the radiation-induced brain injury or damage (RIBI) is partially associated with the sensitivity of particular cell types, pathways of injury in other types of brain disease or damage implicate the significance of the interaction between cell compartments. IRT-induced double-strand breaks (DSBs) are the utmost detrimental kind of DNA damage, which result in cell death as well as sustainable chromosomal reconfigurations following IRT exposure to the brain. It is worth noting that IRT-induced DSBs, and stimulation of interplay of key signaling pathways such as mitogen-activated protein kinases (MAPK), JAK/STAT, phosphoinositide-3-kinase/protein kinase B/AKT (PI3K-PKB/AKT), protein 53 (p53), mammalian target of rapamycin (mTOR), NF-kB, transforming growth factor beta (TGF-

Indexed as

BrainSignal TransductionAnimalsDNA DamageHumansReactive Oxygen SpeciesReactive Oxygen SpeciesimmuneinterplayirradiationradiotherapyRIBIsignaling

Identifiers

PMID41498028
PMCPMC12767455

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.