ArticleCell proliferation2023
Intercellular mitochondrial transfer alleviates pyroptosis in dental pulp damage.
Article in Cell proliferation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- Pioneering next-generation bioactive materials for endodontics: Insights of mitochondrial biology.Bioactive materials · 2026Article
- Redefining the Evolution of Pulpal Pathology: Inflammasomes as Central Integrative Hubs and Biological Switches Governing the Transition From Reversible to Irreversible Pulpal Inflammation Beyond Symptom-Based Classification.International endodontic journal · 2026Review
- Mitochondrial Transport in Bone Metabolism Homeostasis: Molecular Mechanisms and Targeted Therapeutic Strategies.International journal of molecular sciences · 2026Review
- Decoding signaling crosstalk in pulpitis: pathogenesis and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- EPO-modified bone marrow MSCs alleviate asthma inflammation through enhanced mitochondrial activation and transfer by upregulating HO-1.Molecular medicine (Cambridge, Mass.) · 2025Article
- From mitochondria to immune networks: new mesenchymal stem cell strategies to treat periodontitis.Stem cell research & therapy · 2025Review
- NLRP3 Inflammasome-Mediated Pyroptosis in Osteoporosis: Osteoimmune Mechanisms and Therapeutic Targeting.Journal of cellular and molecular medicine · 2025Review
- HDAC9-Mediated Pyroptosis Promotes Orthodontically Induced Inflammatory Root Resorption.International dental journal · 2025Article
- Effect of adipokines on bone marrow mesenchymal stem cell function.World journal of stem cells · 2025Review
- Therapeutic implications of mitochondrial transfer on stem cell fate in regenerative medicine.Journal of translational medicine · 2025Review
- Mitochondria: a key regulator of programmed cell death in OP.Frontiers in endocrinology · 2025Review
- Roles of Pyroptosis in the Progression of Pulpitis and Apical Periodontitis.Journal of inflammation research · 2025Review
- Pyroptosis in Pulpitis.Journal of inflammation research · 2025Review
- Glutamine-αKG axis affects dentin regeneration and regulates osteo/odontogenic differentiation of mesenchymal adult stem cells via IGF2 m6A modification.Stem cell research & therapy · 2024Article
- From dysfunction to healing: advances in mitochondrial therapy for Osteoarthritis.Journal of translational medicine · 2024Review
- Survival advantage of native and engineered T cells is acquired by mitochondrial transfer from mesenchymal stem cells.Journal of translational medicine · 2024Article
- Mitochondrial Dysfunction in the Pathogenesis and Treatment of Oral Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Intercellular mitochondrial transfer alleviates pyroptosis in dental pulp damage.Cell proliferation · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial transfer is emerging as a promising therapeutic strategy for tissue repair, but whether it protects against pulpitis remains unclear. Here, we show that hyperactivated nucleotide-binding domain and leucine-rich repeat protein3 (NLRP3) inflammasomes with pyroptotic cell death was present in pulpitis tissues, especially in the odontoblast layer, and mitochondrial oxidative stress (OS) was involved in driving this NLRP3 inflammasome-induced pathology. Using bone marrow mesenchymal stem cells (BMSCs) as mitochondrial donor cells, we demonstrated that BMSCs could donate their mitochondria to odontoblasts via tunnelling nanotubes (TNTs) and, thus, reduce mitochondrial OS and the consequent NLRP3 inflammasome-induced pyroptosis in odontoblasts. These protective effects of BMSCs were mostly blocked by inhibitors of the mitochondrial function or TNT formation. In terms of the mechanism of action, TNF-α secreted from pyroptotic odontoblasts activates NF-κB signalling in BMSCs via the paracrine pathway, thereby promoting the TNT formation in BMSCs and enhancing mitochondrial transfer efficiency. Inhibitions of NF-κB signalling and TNF-α secretion in BMSCs suppressed their mitochondrial donation capacity and TNT formation. Collectively, these findings demonstrated that TNT-mediated mitochondrial transfer is a potential protective mechanism of BMSCs under stress conditions, suggesting a new therapeutic strategy of mitochondrial transfer for dental pulp repair.
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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 OpenQuestion graph.