Evidence map›Paper›PMID 42496770›Full record

ArticleMolecular biology reports2026

MTA does not induce oxidative stress and apoptotic response, or calcium-related cellular stress and preserves extracellular matrix homeostasis.

Okan Sancer, Deniz Yanık Nalbantoğlu, Ahmet Mert Nalbantoğlu

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Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Okan SancerGenetic Research Unit, Innovative Technologies Application and Research Center, Süleyman Demirel University, Isparta, Turkey.ORCID http://orcid.org/0000-0001-7935-5004
Deniz Yanık NalbantoğluFaculty of Dentistry, Department of Endodontics, Süleyman Demirel University, Isparta, Turkey. deniznalbantoglu@sdu.edu.tr.ORCID http://orcid.org/0000-0001-5676-0293
Ahmet Mert NalbantoğluFaculty of Dentistry, Department of Periodontology, Süleyman Demirel University, Isparta, Turkey.ORCID http://orcid.org/0000-0002-0505-867X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThis study aimed to investigate the time-dependent biological effects of mineral trioxide aggregate (MTA) on cellular viability and the gene expressions associated with oxidative stress response (Nrf2), apoptosis-related signaling (p53), calcium homeostasis (CALB1), and extracellular matrix regulation (FN) in L-929 fibroblasts. METHODS AND

resultsMTA specimens were allowed to set for 4, 6, 8, and 24 h. Eluates were obtained according to ISO-10993-12 guidelines and applied to cells. Cell viability was assessed by MTT assay. Relative mRNA expressions of Nrf2, p53, CALB1, and FN were analyzed by real-time PCR. One-way ANOVA and post-hoc Tukey's were used. Higher cell viability than the positive control was obtained. Viability remained above the 70% biocompatibility threshold in all time periods. A time-dependent fluctuation in viability was observed, with differences between 4 h and 6 h and between 4 h and 8 h (p < 0.05). No significant differences were detected in Nrf2, p53, CALB1, or FN expression levels between the negative control and MTA-treated groups at any time point (p > 0.05).

conclusionMTA preserved cellular viability and molecular homeostasis without inducing oxidative, apoptotic, or calcium-related imbalance. The inclusion of Nrf2 and CALB1 as previously unexplored parameters provides additional mechanistic insight into the biocompatibility profile of MTA. MTA maintained cellular homeostasis throughout its critical setting phase without activating oxidative stress, apoptosis-related signaling, or calcium imbalance pathways. The stable expression of Nrf2, p53, and CALB1 suggests that the favorable clinical performance may depend not only on biocompatibility but also on its ability to preserve intracellular equilibrium during early tissue contact.

Indexed as

Aluminum CompoundsCalciumCalcium CompoundsExtracellular MatrixOxidative StressOxidesSilicatesAnimalsApoptosisCell LineCell SurvivalDrug CombinationsFibroblastsHomeostasisHumansNF-E2-Related Factor 2Aluminum CompoundsCalciumCalcium CompoundsDrug Combinationsmineral trioxide aggregateNF-E2-Related Factor 2OxidesSilicatesTumor Suppressor Protein p53ApoptosisEndodonticsExtracellular matrixMineral trioxide aggregateOxidative stress

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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.