Evidence map›Paper›PMID 29872395›Full record

ReviewFrontiers in pharmacology2018

Ionizing Radiation-Induced Cellular Senescence in Normal, Non-transformed Cells and the Involved DNA Damage Response: A Mini Review.

Mengqian Li, Liting You, Jianxin Xue, You Lu

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
9.4field-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

81 citing papers in PubMed, 122 citations in OpenAlex.

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  15. Downregulation of EZH2 Promotes Renal Epithelial Cellular Senescence and Kidney Aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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21 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 1 institution in 1 country.

Mengqian LiDepartment of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Liting YouDepartment of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Jianxin XueDepartment of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
You LuDepartment of Thoracic Oncology, Cancer Center, West China Hospital, Sichuan University, Chengdu, China.
Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is identified by a living cell in irreversible and persistent cell cycle arrest in response to various cellular stresses. Senescent cells secrete senescence-associated secretory phenotype factors that can amplify cellular senescence and alter the microenvironments. Radiotherapy, via ionizing radiation, serves as an effective treatment for local tumor control with side effects on normal cells, which can induce inflammation and fibrosis in irradiated and nearby regions. Research has revealed that senescent phenotype is observable in irradiated organs. This process starts with DNA damage mediated by radiation, after which a G2 arrest occurs in virtually all eukaryotic cells and a mitotic bypass is possibly necessary to ultimately establish cellular senescence. Within this complex DNA damage response signaling network, ataxia telangiectasia-mutated protein, p53, and p21 stand out as the crucial mediators. Senolytic agents, a class of small molecules that can selectively kill senescent cells, hold great potential to substantially reduce the side effects caused by radiotherapy while reasonably steer clear of carcinogenesis.

Indexed as

cell cyclecellular senescenceDNA damageionizing radiationsenolytic

Identifiers

PMID29872395
PMCPMC5972185
OpenAlexW2800321821

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.