Evidence map›Paper›PMID 35075260›Full record

ArticleScientific reports2022

Intracellular glucose starvation affects gingival homeostasis and autophagy.

Runbo Li, Hirohito Kato, Yoichiro Taguchi, Makoto Umeda

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

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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 1 institution in 1 country.

Runbo LiDepartment of Periodontology, Osaka Dental University, 8-1, Kuzuhahanazono-cho, Hirakata, Osaka, Japan.
Hirohito KatoDepartment of Periodontology, Osaka Dental University, 8-1, Kuzuhahanazono-cho, Hirakata, Osaka, Japan.
Yoichiro TaguchiDepartment of Periodontology, Osaka Dental University, 8-1, Kuzuhahanazono-cho, Hirakata, Osaka, Japan. taguchi@cc.osaka-dent.ac.jp.
Makoto UmedaDepartment of Periodontology, Osaka Dental University, 8-1, Kuzuhahanazono-cho, Hirakata, Osaka, Japan.
Osaka Dental University · JP

Funding

Japan Society for the Promotion of Science No. 21K09946
6 · The paper itself

Abstract

Human gingival fibroblasts (HGnFs) maintain periodontal tissue homeostasis through active proliferation and migration. Clinically, it is considered that the wound-healing ability of the gingival tissue is maintained even in environments with insufficient supply of nutrients, such as glucose, immediately after periodontal surgery. However, the effects of such glucose-deficient environments on HGnFs remain unclear. This study aimed to investigate the effects of low-glucose environment on HGnFs homeostasis. We evaluated gingival wound healing by examining cell proliferation and migration and collagen synthesis in HGnFs cultured in 100, 50, 25, and 0 mg/dL glucose in vitro. The cellular stress levels were determined by measuring the lactate dehydrogenase (LDH) and reactive oxygen species (ROS) levels. The glucose metabolism of HGnFs in the low-glucose concentrations was studied by measuring glucose transporter type 1 (GLUT1) mRNA expression, glucose uptake assays, lactate and ATP productions. Molecular effects were examined with a focus on the LKB1-AMPK signaling pathway. Autophagy activity in glucose-deprived HGnFs was evaluated by measuring the levels of autophagy-related proteins. Low glucose levels increased cellular stress levels, autophagy activity, and enhanced glucose metabolism through the LKB1-AMPK signaling pathway, providing more ATPs to promote wound healing. Our results regarding glucose transfer suggest the rapid healing of gingival wounds.

Indexed as

AutophagyWound HealingAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesCells, CulturedFibroblastsGingivaGlucoseGlycolysisHumansAMP-Activated Protein Kinase KinasesAMP-Activated Protein KinasesGlucoseSTK11 protein, human

Identifiers

PMID35075260
PMCPMC8786886
OpenAlexW4206969118

What OpenQuestion holds

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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.