ArticleExperimental and therapeutic medicine2020
Induction of autophagy protects human dental pulp cells from lipopolysaccharide-induced pyroptotic cell death.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Role of Lipopolysaccharide, Derived from Various Bacterial Species, in Pulpitis-A Systematic Review.Biomolecules · 2022Pooled it
- Protein Kinase R-like Endoplasmic Reticulum Kinase-Mediated ER-Mitochondria Coupling Regulates Odontogenic Differentiation of Human Dental Pulp Stem Cells Under Inflammatory Stimuli.International dental journal · 2026Article
- High glucose impairs autophagy and mitochondrial homeostasis in human dental pulp cells.Scientific reports · 2026Article
- Mechanobiological and Molecular Alterations in the Aging Dentin-Pulp Complex.Life (Basel, Switzerland) · 2026Article
- Lipopolysaccharides Modulate Cellular Responses in Dental Pulp Cells.International journal of dentistry · 2026Review
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- Pyroptosis in Pulpitis.Journal of inflammation research · 2025Review
- Transcriptome profiling of DPP stimulated DPSCs identifies the role of autophagy in odontogenic differentiation.Journal of structural biology · 2024Article
- BRF1 promotes the odontogenic differentiation of dental pulp stem cells in pulpitis by inducing autophagy.Heliyon · 2024Article
- Dental Stem Cells and Lipopolysaccharides: A Concise Review.International journal of molecular sciences · 2024Review
- Long-term passage impacts human dental pulp stem cell activities and cell response to drug additionPeerJ · 2024Article
- Effect of cryotherapy duration on experimentally induced connective tissue inflammationRestorative dentistry & endodontics · 2023Article
- TPPU inhibits inflammation-induced excessive autophagy to restore the osteogenic differentiation potential of stem cells and improves alveolar ridge preservation.Scientific reports · 2023Article
- LPS-induced autophagy in human dental pulp cells is associated with p38.Journal of molecular histology · 2021Article
- Injectable Multifunctional Drug Delivery System for Hard Tissue Regeneration under Inflammatory Microenvironments.ACS applied bio materials · 2021Article
- Autophagy blockage promotes the pyroptosis of ox-LDL-treated macrophages by modulating the p62/Nrf2/ARE axis.Journal of physiology and biochemistry · 2021Article
- Autophagy, Pyroptosis, and Ferroptosis: New Regulatory Mechanisms for Atherosclerosis.Frontiers in cell and developmental biology · 2021Review
- Rapamycin Inhibited Pyroptosis and Reduced the Release of IL-1BioMed research international · 2020Article
- Unravelling the role of autophagy in human dental pulp.Journal of oral and maxillofacial pathology : JOMFPArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NOD-like receptor protein 3/caspase-1 inflammasome can be activated in human dental pulp tissue and fibroblasts; however, the underlying mechanisms are poorly understood. In the present study, lipopolysaccharide (LPS) was used to treat dental pulp cells to establish an inflammation model. Cell viability was examined by sulforhodamine B assay. Interleukin (IL)-1β, caspase-1, microtubule-associated protein-1 light chain 3-II/I and p62 were determined by western blotting and ELISA. The phosphorylation (p-) levels of NF-κB and NF-κB inhibitor (IκB)α protein were observed by western blotting. The results demonstrated that LPS induced pyroptotic cell death in cultured dental pulp cells, which was supported by the increased levels of IL-1β, IL-18 and caspase-1. Rapamycin and 3-methyladenine (3-MA) were used to activate and inhibit autophagy, and it was observed that LPS increased autophagy and rapamycin reduced LPS-induced dental pulp cell pyroptosis. However, 3-MA aggravated LPS-induced dental pulp cell pyroptosis. In addition, LPS inhibited the expression of IκBα, but increased the expression of p-NF-κB. Compared with the LPS group, 3-MA further inhibited the expression of IκBα but promoted the expression of p-NF-κB. However, rapamycin produced the opposite results to LPS. Under LPS treatment, the NF-κB pathway inhibitor BAY11-7082 further enhanced the inhibitory effects of rapamycin, but inhibited the promoting effects of 3-MA on the protein expression levels of IL-1β and caspase-1. The results of the present study demonstrated that there is an important crosstalk between autophagy, pyroptosis and the NF-κB pathway, and that the modulation of pyroptosis in dental pulp cells may be a promising strategy to pulpitis therapy.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.