Evidence map›Paper›PMID 37641630›Full record

ArticleFrontiers in dental medicine2022

Prolyl-hydroxylase inhibitor-induced regeneration of alveolar bone and soft tissue in a mouse model of periodontitis through metabolic reprogramming.

Elan Zebrowitz, Azamat Aslanukov, Tetsuhiro Kajikawa, Kamila Bedelbaeva, Sam Bollinger, Yong Zhang, David Sarfatti, Jing Cheng, Phillip B Messersmith, George Hajishengallis and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in dental medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
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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

11 authors at 4 institutions in 1 country.

Elan ZebrowitzLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Azamat AslanukovLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Tetsuhiro KajikawaUniversity of Pennsylvania School of Dental Medicine, Department of Basic and Translational Sciences, Philadelphia, Pennsylvania, United States of America.
Kamila BedelbaevaLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Sam BollingerLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Yong ZhangLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
David SarfattiLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Jing ChengMaterials Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California, United States of America.
Phillip B MessersmithDepartment of Bioengineering and Materials Science and Engineering, UC Berkeley, Berkeley California, United States of America.
George HajishengallisUniversity of Pennsylvania School of Dental Medicine, Department of Basic and Translational Sciences, Philadelphia, Pennsylvania, United States of America.
Ellen Heber-KatzLankenau Institute for Medical Research, Wynnewood, Pennsylvania, United States of America.
Lankenau Institute for Medical Research · USUniversity of Pennsylvania · USLawrence Berkeley National Laboratory · USUniversity of California, Berkeley · US

Funding

Regenerative wound healing via inflammation-modulating biomaterialsR01DE021104 · NIDCR · WISTAR INSTITUTE · PI Georgios Hajishengallis, Ellen s. Heber-Katz · 2011 to 2026
$8.5M
NIDCR NIH HHS R01 DE021104
6 · The paper itself

Abstract

Bone injuries and fractures reliably heal through a process of regeneration with restoration to original structure and function when the gap between adjacent sides of a fracture site is small. However, when there is significant volumetric loss of bone, bone regeneration usually does not occur. In the present studies, we explore a particular case of volumetric bone loss in a mouse model of human periodontal disease (PD) in which alveolar bone surrounding teeth is permanently lost and not replaced. This model employs the placement a ligature around the upper second molar for 10 days leading to inflammation and bone breakdown and faithfully replicates the bacterially-induced inflammatory etiology of human PD to induce bone degeneration. After ligature removal, mice are treated with a timed-release formulation of a small molecule inhibitor of prolylhydroxylases (PHDi; 1,4-DPCA) previously shown to induce epimorphic regeneration of soft tissue in non-regenerating mice. This PHDi induces high expression of HIF-1α and is able to shift the metabolic state from OXPHOS to aerobic glycolysis, an energetic state used by stem cells and embryonic tissue. This regenerative response was completely blocked by

Indexed as

1,4-DPCAAlveolar BoneGapdhGlut-1HIF-1αLdh-a: Micro-CTMiceOCT3/4Pdk1Periodontal DiseasePeriodontal LigamentPgk1PHDiPulp

Identifiers

PMID37641630
PMCPMC10462383
OpenAlexW4310040932

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.