ArticleCell death and differentiation2016
Decreased MORF leads to prolonged endoplasmic reticulum stress in periodontitis-associated chronic inflammation.
Article in Cell death and differentiation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 76 citations in OpenAlex.
- MAPK Phosphatase-3 Mediates Chronic Endoplasmic Reticulum Stress Promoting Hepatic Gluconeogenesis.International journal of molecular sciences · 2026Article
- L-Glutamate enables the EGFR-MEK-ERK-mTFB2 axis to enhance mitochondrial biogenesis in intestinal stem cells.Stem cell research & therapy · 2025Article
- Impaired stemness in aging periodontal ligament stem cells is mediated by the progerin/endoplasmic reticulum stress/p53 axis.Journal of advanced research · 2025Article
- Stepwise Administration of Bone-Targeted Lipid Nanoparticles Encapsulating Valproic Acid and TUDCA Facilitates In Vivo Direct Reprogramming for Osteoporosis Treatment.Tissue engineering and regenerative medicine · 2025Article
- Identification and validation of endoplasmic reticulum autophagy-related potential biomarkers in periodontitis.Scientific reports · 2025Article
- M2 macrophage-derived mitochondrial transplantation promotes periodontal bone regeneration by regulating metabolic homeostasis via activating p38-MAPK signaling pathway.Stem cell research & therapy · 2025Article
- ERS-PERK Pathway is Involved in the Repair of the Pulpo-Dentinal Complex Under an Inflammatory Microenvironment.Stem cells international · 2025Article
- Discovering common pathogenetic processes between periodontitis and Alzheimer's disease by bioinformatics and system biology approach.BMC oral health · 2024Article
- Nanoparticles in Periodontitis Therapy: A Review of the Current Situation.International journal of nanomedicine · 2024Review
- Mitochondria in Multi-Directional Differentiation of Dental-Derived Mesenchymal Stem Cells.Biomolecules · 2023Review
- Article
- Melatonin Engineering M2 Macrophage-Derived Exosomes Mediate Endoplasmic Reticulum Stress and Immune Reprogramming for Periodontitis Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Endoplasmic reticulum stress: a novel targeted approach to repair bone defects by regulating osteogenesis and angiogenesis.Journal of translational medicine · 2023Review
- Regulatory mechanisms of GCN5 in osteogenic differentiation of MSCs in periodontitis.Clinical and experimental dental research · 2023Review
- Role of Berberine Thermosensitive Hydrogel in Periodontitis via PI3K/AKT Pathway In Vitro.International journal of molecular sciences · 2023Article
- Mesenchymal stem cells: Emerging concepts and recent advances in their roles in organismal homeostasis and therapy.Frontiers in cellular and infection microbiology · 2023Review
- Review
- Bone regeneration strategies based on organelle homeostasis of mesenchymal stem cells.Frontiers in endocrinology · 2023Review
- Glycolytic reprogramming in macrophages and MSCs during inflammation.Frontiers in immunology · 2023Article
- Dexamethasone-loaded zeolitic imidazolate frameworks nanocomposite hydrogel with antibacterial and anti-inflammatory effects for periodontitis treatment.Materials today. Bio · 2022Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The association between inflammation and endoplasmic reticulum (ER) stress has been described in many diseases. However, if and how chronic inflammation governs the unfolded protein response (UPR) and promotes ER homeostasis of chronic inflammatory disease remains elusive. In this study, chronic inflammation resulted in ER stress in mesenchymal stem cells in the setting of periodontitis. Long-term proinflammatory cytokines induced prolonged ER stress and decreased the osteogenic differentiation of periodontal ligament stem cells (PDLSCs). Interestingly, we showed that chronic inflammation decreases the expression of lysine acetyltransferase 6B (KAT6B, also called MORF), a histone acetyltransferase, and causes the upregulation of a key UPR sensor, PERK, which lead to the persistent activation of the UPR in PDLSCs. Furthermore, we found that the activation of UPR mediated by MORF in chronic inflammation contributes to the PERK-related deterioration of the osteogenic differentiation of PDLSCs both in vivo and in vitro. Taken together, our results suggest that chronic inflammation compromises UPR function through MORF-mediated-PERK transcription, which is a previously unrecognized mechanism that contributes to impaired ER function, prolonged ER stress and defective osteogenic differentiation of PDLSCs in periodontitis.
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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.