Evidence map›Paper›PMID 29654284›Full record

ArticleInternational journal of oral science2018

Activation of hypoxia-inducible factor 1 attenuates periapical inflammation and bone loss.

Kimito Hirai, Hisako Furusho, Kiichi Hirota, Hajime Sasaki

Open access · goldAbstract read
In one paragraph

Article in International journal of oral science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

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  17. Potential mechanism of ginseng in the treatment of periodontitis based on network pharmacology and molecular docking.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2024
    Article
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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

4 authors at 3 institutions in 2 countries.

Kimito HiraiDepartment of Cariology, Restorative Sciences & Endodontics, University of Michigan School of Dentistry, Ann Arbor, MI, USA.
Hisako FurushoDepartment of Oral and Maxillofacial Pathobiology, Hiroshima University, Hiroshima, Hiroshima, Japan.
Kiichi HirotaDepartment of Human Stress Response Science, Institute of Biomedical Science, Kansai Medical University, Hirakata, Osaka, Japan.
Hajime SasakiDepartment of Cariology, Restorative Sciences & Endodontics, University of Michigan School of Dentistry, Ann Arbor, MI, USA. hajimes@umich.edu.
Hiroshima University · JPKansai Medical University · JPUniversity of Michigan–Ann Arbor · US

Funding

Functional role of Serum Amyloid A in periapical inflammationR01DE024796 · NIDCR · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI SASAKI, HAJIME · 2015 to 2020
$2.1M
HIF-1alpha Mediated Wound Healing in Periapical LesionR21DE023178 · NIDCR · ADA FORSYTH INSTITUTE, INC. · PI SASAKI, HAJIME · 2013 to 2014
$542k
MicroCT Core Facility in the Forsyth InstituteS10RR027553 · NCRR · ADA FORSYTH INSTITUTE, INC. · PI SASAKI, HAJIME · 2010 to 2010
$295k
NCRR NIH HHS S10 RR027553NIDCR NIH HHS R01 DE024796NIDCR NIH HHS R21 DE023178
6 · The paper itself

Abstract

Hypoxia (low oxygen level) is an important feature during infections and affects the host defence mechanisms. The host has evolved specific responses to address hypoxia, which are strongly dependent on the activation of hypoxia-inducible factor 1 (HIF-1). Hypoxia interferes degradation of HIF-1 alpha subunit (HIF-1α), leading to stabilisation of HIF-1α, heterodimerization with HIF-1 beta subunit (HIF-1β) and subsequent activation of HIF-1 pathway. Apical periodontitis (periapical lesion) is a consequence of endodontic infection and ultimately results in destruction of tooth-supporting tissue, including alveolar bone. Thus far, the role of HIF-1 in periapical lesions has not been systematically examined. In the present study, we determined the role of HIF-1 in a well-characterised mouse periapical lesion model using two HIF-1α-activating strategies, dimethyloxalylglycine (DMOG) and adenovirus-induced constitutively active HIF-1α (CA-HIF1A). Both DMOG and CA-HIF1A attenuated periapical inflammation and tissue destruction. The attenuation in vivo was associated with downregulation of nuclear factor-κappa B (NF-κB) and osteoclastic gene expressions. These two agents also suppressed NF-κB activation and subsequent production of proinflammatory cytokines by macrophages. Furthermore, activation of HIF-1α by DMOG specifically suppressed lipopolysaccharide-stimulated macrophage differentiation into M1 cells, increasing the ratio of M2 macrophages against M1 cells. Taken together, our data indicated that activation of HIF-1 plays a protective role in the development of apical periodontitis via downregulation of NF-κB, proinflammatory cytokines, M1 macrophages and osteoclastogenesis.

Indexed as

Alveolar Bone LossAmino Acids, DicarboxylicAnimalsCytokinesDown-RegulationGene ExpressionHypoxia-Inducible Factor 1, alpha SubunitMacrophagesMiceNF-kappa BOsteogenesisPeriapical PeriodontitisReal-Time Polymerase Chain ReactionX-Ray MicrotomographyAmino Acids, DicarboxylicCytokinesHypoxia-Inducible Factor 1, alpha SubunitNF-kappa Boxalylglycine

Identifiers

PMID29654284
PMCPMC5966812
OpenAlexW2803347716

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.