ArticleInternational dental journal2026
MT2A-Mediated Regulation of Cuproptosis in Human Dental Pulp Cells Modulates Macrophage M1 Polarization in Pulpitis.
Article in International dental journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe progression of pulpitis is strongly affected by the fate of dental pulp cells, with their modes of cell death determining whether inflammation resolves or leads to irreversible necrosis. Cuproptosis, a copper-dependent form of regulated cell death, has been implicated in inflammatory and metabolic disorders. Given the high metabolic activity of pulp cells and dynamic copper fluctuations during inflammation, cuproptosis may play a role in pulpitis, though this remains unexplored.
methodsCopper deposition was examined in inflamed dental pulp using copper staining, and cuproptosis activation was assessed by lipoylated Dihydrolipoamide S-acetyltransferase (lip-DLAT) expression through Western blot (WB) and immunofluorescence (IF). Key cuproptosis-related genes, including Metallothionein 2A (MT2A), were identified from Gene Expression Omnibus (GEO) datasets and validated. A mouse pulpitis model with MTII (MT2A ortholog in mouse) knockdown was used to evaluate pulp tissue changes via Hematoxylin and Eosin staining and IF staining, and immune infiltration analyses were performed to identify MT2A-related immune cells. Finally, an inflammatory human dental pulp cells (hDPCs) model was used to assess its effects on macrophages by flow cytometry.
resultsInflamed human pulp tissues exhibited marked copper accumulation and significantly elevated lip-DLAT expression, indicating activation of cuproptosis. Bioinformatic analysis of GEO datasets identified 6 hub cuproptosis-related genes, which were validated by reverse transcription quantitative polymerase chain reaction. In hDPCs, the cuproptosis inhibitor tetrathiomolybdate reduced copper overload, cell death, and lip-DLAT expression. Conversely, MT2A knockdown enhanced cuproptosis, as evidenced by increased copper accumulation, lip-DLAT levels, and IL-6 expression. Moreover, MT2A knockdown in the inflammatory hDPCs model promoted M1 macrophage polarization.
conclusionCuproptosis is activated in inflamed dental pulp and contributes to the pathogenesis of pulpitis. MT2A functions as a protective regulator, mitigating cuproptosis and modulating macrophage-mediated inflammatory responses. Targeting cuproptosis and MT2A may represent a novel therapeutic strategy for preserving pulp vitality.
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.