Evidence map›Paper›PMID 27459704›Full record

ArticleRadiation research2016

Radiation-Induced Microvascular Injury as a Mechanism of Salivary Gland Hypofunction and Potential Target for Radioprotectors.

Aviram Mizrachi, Ana P Cotrim, Nora Katabi, James B Mitchell, Marcel Verheij, Adriana Haimovitz-Friedman

Open access · greenAbstract read
In one paragraph

Article in Radiation research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

31 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  3. Organoid-based modeling and regenerative strategies for salivary gland dysfunction.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

6 authors at 1 institution in 1 country.

Aviram MizrachiDepartments of a Surgery, Head and Neck Service.
Ana P Cotrimd Radiation Biology Branch, National Cancer Institute, National Institute of Health, Bethesda, Maryland; and.
Nora Katabib Pathology and.
James B Mitchelld Radiation Biology Branch, National Cancer Institute, National Institute of Health, Bethesda, Maryland; and.
Marcel Verheije Department of Radiation Oncology, Netherlands Cancer Institute, Amsterdam.
Adriana Haimovitz-Friedmanc Radiation Oncology, Memorial Sloan-Kettering Cancer Center, New York, New York;
Memorial Sloan Kettering Cancer Center · US

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI Hongbiao Carl Lekaye · 1985 to 2026
$347.4M
Intramural NIH HHS Z99 CA999999NCI NIH HHS P30 CA008748
6 · The paper itself

Abstract

Radiation therapy is commonly used to treat patients with head and neck squamous cell carcinoma (HNSCC). One of the major side effects of radiotherapy is injury to the salivary glands (SG), which is thought to be mediated by microvascular dysfunction leading to permanent xerostomia. The goal of this study was to elucidate the mechanism of radiation-induced microvasculature damage and its impact on SG function. We measured bovine aortic endothelial cell (BAEC) apoptosis and ceramide production in response to 5 Gy irradiation, either alone or with reactive oxygen species (ROS) scavengers. We then investigated the effect of a single 15 Gy radiation dose on murine SG function. BAECs exposed to 5 Gy underwent apoptosis with increased ceramide production, both prevented by ROS scavengers. Among the 15 Gy irradiated mice, there was considerable weight loss, alopecia and SG hypofunction manifested by reduced saliva production and lower lysozyme levels. All of these effects, except for the lysozyme levels, were prevented by pretreatment with ROS scavengers. Microvessel density was significantly lower in the SG of irradiated mice compared to the control group, and this effect was significantly attenuated by pretreatment with Tempol. This study demonstrates that radiation-induced SG hypofunction is to a large extent mediated by microvascular dysfunction involving ceramide and ROS generation. These findings strongly suggest that ROS scavengers may serve as potential radioprotectors of SG function in patients undergoing radiotherapy for HNSCC.

Indexed as

AnimalsApoptosisCattleCeramidesEndothelium, VascularFemaleFree Radical ScavengersMiceMicrovesselsRadiation-Protective AgentsReactive Oxygen SpeciesSalivary GlandsTime FactorsCeramidesFree Radical ScavengersRadiation-Protective AgentsReactive Oxygen Species

Identifiers

PMID27459704
PMCPMC5134326
OpenAlexW2498275671

What OpenQuestion holds

Textmetadata
LicenceTDM
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.