Evidence map›Paper›PMID 25323788›Full record

ArticleExperimental & molecular medicine2014

Chronic stress enhances progression of periodontitis via α1-adrenergic signaling: a potential target for periodontal disease therapy.

Huaixiu Lu, Minguang Xu, Feng Wang, Shisen Liu, Jing Gu, Songshan Lin

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 37% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Noradrenaline Synergistically EnhancesInternational journal of molecular sciences · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. 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

6 authors at 2 institutions in 1 country.

Huaixiu LuDepartment of Stomatology, Navy General Hospital, Beijing, China.
Minguang XuDepartment of Medical Engineering, The Second Artillery General Hospital of PLA, Beijing, China.
Feng WangDepartment of Stomatology, Navy General Hospital, Beijing, China.
Shisen LiuDepartment of Stomatology, Navy General Hospital, Beijing, China.
Jing GuDepartment of Stomatology, Navy General Hospital, Beijing, China.
Songshan LinDepartment of Stomatology, Navy General Hospital, Beijing, China.
PLA Navy General Hospital · CNSecond Artillery General Hospital of Chinese People's Liberation Army · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study assessed the roles of chronic stress (CS) in the stimulation of the sympathetic nervous system and explored the underlying mechanisms of periodontitis. Using an animal model of periodontitis and CS, the expression of tyrosine hydroxylase (TH) and the protein levels of the α1-adrenergic receptor (α1-AR) and β2-adrenergic receptor (β2-AR) were assessed. Furthermore, human periodontal ligament fibroblasts (HPDLFs) were stimulated with lipopolysaccharide (LPS) to mimic the process of inflammation. The proliferation of the HPDLFs and the expression of α1-AR and β2-AR were assessed. The inflammatory-related cytokines interleukin (IL)-1β, IL-6 and IL-8 were detected after pretreatment with the α1/β2-AR blockers phentolamine/propranolol, both in vitro and in vivo. Results show that periodontitis under CS conditions enhanced the expression of TH, α1-AR and β2-AR. Phentolamine significantly reduced the inflammatory cytokine levels. Furthermore, we observed a marked decrease in HPDLF proliferation and the increased expression of α1-ARfollowing LPS pretreatment. Pretreatment with phentolamine dramatically ameliorated LPS-inhibited cell proliferation. In addition, the blocking of α1-ARsignaling also hindered the upregulation of the inflammatory-related cytokines IL-1β, IL-6 and IL-8. These results suggest that CS can significantly enhance the pathological progression of periodontitis by an α1-adrenergic signaling-mediated inflammatory response. We have identified a potential therapeutic target for the treatment of periodontal disease, particularly in those patients suffering from concurrent CS.

Indexed as

Stress, PhysiologicalAdrenergic alpha-1 Receptor AntagonistsAnimalsCells, CulturedCytokinesFibroblastsHumansLipopolysaccharidesMalePeriodontal LigamentPeriodontitisPhentolamineRatsRats, WistarReceptors, Adrenergic, alpha-1Signal TransductionAdrenergic alpha-1 Receptor AntagonistsCytokinesLipopolysaccharidesPhentolamineReceptors, Adrenergic, alpha-1Tyrosine 3-Monooxygenase

Identifiers

PMID25323788
PMCPMC4221694
OpenAlexW2044433483

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.