Evidence map›Paper›PMID 34309809›Full record

ArticleJournal of molecular histology2021

LPS-induced autophagy in human dental pulp cells is associated with p38.

Yihua Huang, Xuyan Li, Yiwen Liu, Qimei Gong, Jun Tian, Hongwei Jiang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Role of Autophagy in the Mineralization Process of Bone and Dentin.International journal of molecular sciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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 3 institutions in 1 country.

Yihua HuangDepartment of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China.
Xuyan LiDepartment of Operative Dentistry and Endodontics, Stomatology, Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Tongji University, Shanghai, 20072, China.
Yiwen LiuDepartment of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China.
Qimei GongDepartment of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China.
Jun TianDepartment of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China.
Hongwei JiangDepartment of Operative Dentistry and Endodontics, Hospital of Stomatology, Guanghua School of Stomatology, Sun Yat-sen University, 56 Ling yuan Road West, Guangzhou, 510055, China. jianghw@163.com.
Stomatology Hospital · CNSun Yat-sen University · CNTongji University · CN

Funding

National Natural Science Foundation of China 81700957National Natural Science Foundation of China 81800750Natural Science Foundation of Guangdong Province 2016A030310197
6 · The paper itself

Abstract

Lipopolysaccharides (LPS), which are components of the cell wall of Gram-negative bacteria, are among the important factors that induce inflammation, including pulpitis. Autophagy in human dental pulp cells (hDPCs) acts as a protective mechanism that promotes cell survival under adverse conditions through different signaling pathways. In this study, we examined whether LPS increases autophagy in hDPCs and investigated the role of mitogen-activated protein kinases signaling and nuclear factor κB (NF-κB) in this process. We found that stimulation of hDPCs with 0.1 µg/mL LPS increased the protein and mRNA levels of autophagy markers, beclin1 and microtubule associated protein light chain 3II (LC3II). In addition, acridine orange staining and transmission electron microscopy demonstrated the induction of autophagy upon the treatment of LPS. Furthermore, LPS affected phosphorylation of p38, extracellular signal-regulated kinase (ERK), and c-Jun N-terminal kinase (JNK), and the nuclear translocation of NF-κB. While p38 inhibitor suppressed the LPS-induced increase in protein levels of beclin1 and LC3-II. Our results suggest that LPS induced autophagy in hDPCs and affected the phosphorylation of p38, ERK, and JNK, as well as the nuclear translocation of NF-κB. Phosphorylation of p38 may be involved in LPS-induced autophagy in hDPCs.

Indexed as

AutophagyAdolescentAdultBeclin-1Dental PulpHumansLipopolysaccharidesLysosomesMAP Kinase Signaling SystemMicrotubule-Associated ProteinsNF-kappa Bp38 Mitogen-Activated Protein KinasesRNA, MessengerVacuolesYoung AdultBeclin-1LipopolysaccharidesMAP1LC3A protein, humanMicrotubule-Associated ProteinsNF-kappa Bp38 Mitogen-Activated Protein KinasesRNA, MessengerAutophagyHuman dental pulp cellsLipopolysaccharidesp38

Identifiers

PMID34309809
OpenAlexW3184375655

What Socratic holds

Textmetadata
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 Socratic graph.