Evidence map›Paper›PMID 36130514›Full record

ArticleCell reports2022

Targeting the succinate receptor effectively inhibits periodontitis.

Yuqi Guo, Fangxi Xu, Scott C Thomas, Yanli Zhang, Bidisha Paul, Satish Sakilam, Sungpil Chae, Patty Li, Caleb Almeter, Angela R Kamer and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Metabolic Reprogramming of Macrophages Plays a Dual Role in Periodontitis: From Pathogenesis to Therapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Vascular changes and their implications in lipedema.Frontiers in cell and developmental biology · 2026
    Review
  8. Review
  9. Review
  10. Emerging roles of the metabolite succinate in bone-related diseases.Journal of Zhejiang University. Science. B · 2025
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Metabolic Footprint ofPathogens (Basel, Switzerland) · 2024
    Article
  17. Article
  18. Review
  19. Article
  20. Article
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

14 authors at 3 institutions in 1 country.

Yuqi GuoDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Fangxi XuDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Scott C ThomasDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Yanli ZhangDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Bidisha PaulDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Satish SakilamDepartment of Chemistry, New York University, New York, NY 10003, USA.
Sungpil ChaeDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Patty LiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Caleb AlmeterDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA.
Angela R KamerDepartment of Periodontology and Implant Dentistry, New York University College of Dentistry, New York, NY 10010, USA.
Paramjit AroraDepartment of Chemistry, New York University, New York, NY 10003, USA.
Dana T GravesDepartment of Periodontics, University of Pennsylvania School of Dental Medicine, Philadelphia, PA 19104, USA.
Deepak SaxenaDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA; Department of Surgery, New York University Grossman School of Medicine, New York, NY 10016, USA. Electronic address: ds100@nyu.edu.
Xin LiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, NY 10010, USA; Department of Urology, New York University Grossman School of Medicine, New York, NY 10016, USA; Perlmutter Cancer Institute, New York University Langone Medical Center, New York, NY 10016, USA. Electronic address: xl15@nyu.edu.
New York University · USNYU Langone Health · USUniversity of Pennsylvania · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI MARK Reid PHILIPS · 1985 to 2026
$83.1M
Diabetes-enhanced Experimental PeriodontitisR01DE017732 · NIDCR · UNIV OF MED/DENT OF NJ-NJ DENTAL SCHOOL · PI DANA T GRAVES · 2007 to 2026
$6.5M
Targeting Succinate Signaling Impedes Periodontitis ProgressionR01DE027074 · NIDCR · NEW YORK UNIVERSITY · PI GRAVES, DANA T, LI, XIN · 2018 to 2022
$2.6M
Succinate triggers gut dysbiosis and activates SUCNR1 to enhance inflammagingR01AG068857 · NIA · UNIVERSITY OF VIRGINIA · PI LI, XIN, SAXENA, DEEPAK · 2020 to 2024
$2.4M
A Novel Remedy for Periodontal Bone LossR42DE028212 · NIDCR · PERIOMICS CARE, LLC · PI LI, XIN, SAXENA, DEEPAK · 2022 to 2023
$1.6M
A Novel remedy for periodontal bone lossR41DE028212 · NIDCR · PERIOMICS CARE, LLC · PI LI, XIN, SAXENA, DEEPAK · 2019 to 2019
$224k
NCI NIH HHS P30 CA016087NIA NIH HHS R01 AG068857NIDCR NIH HHS R01 DE017732NIDCR NIH HHS R01 DE027074NIDCR NIH HHS R41 DE028212NIDCR NIH HHS R42 DE028212
6 · The paper itself

Abstract

Periodontal disease (PD) is one of the most common inflammatory diseases in humans and is initiated by an oral microbial dysbiosis that stimulates inflammation and bone loss. Here, we report an abnormal elevation of succinate in the subgingival plaque of subjects with severe PD. Succinate activates succinate receptor-1 (SUCNR1) and stimulates inflammation. We detected SUCNR1 expression in the human and mouse periodontium and hypothesize that succinate activates SUCNR1 to accelerate periodontitis through the inflammatory response. Administration of exogenous succinate enhanced periodontal disease, whereas SUCNR1 knockout mice were protected from inflammation, oral dysbiosis, and subsequent periodontal bone loss in two different models of periodontitis. Therapeutic studies demonstrated that a SUCNR1 antagonist inhibited inflammatory events and osteoclastogenesis in vitro and reduced periodontal bone loss in vivo. Our study reveals succinate's effect on periodontitis pathogenesis and provides a topical treatment for this disease.

Indexed as

Alveolar Bone LossPeriodontal DiseasesPeriodontitisAnimalsDysbiosisHumansInflammationMiceMice, KnockoutSuccinic AcidSuccinic Acidbone lossCP: MicrobiologyinflammationmicrobiomeperiodontitissuccinateSUCNR1therapeutics

Identifiers

PMID36130514
PMCPMC9533417
OpenAlexW4296799497

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.