ArticleAnnals of translational medicine2022
SDHB reduction promotes oral lichen planus by impairing mitochondrial respiratory function.
Article in Annals of translational medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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The trial behind it
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 citations in OpenAlex.
- Aberrant Energy Metabolism in Tumors and Potential Therapeutic Targets.Genes, chromosomes & cancer · 2024Pooled it
- Causal Associations Between Chronic Inflammatory Skin Diseases and Alzheimer's Disease: A Bidirectional Two-Sample Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- Oxidative stress and metabolic dysfunction in oral lichen planus pathogenesis.Animal cells and systems · 2026Review
- Bacterial Extracellular Vesicles as Potential Promoting Factors for Oral Lichen Planus Pathogenesis.Inflammation · 2025Article
- Prediction model of mitochondrial energy metabolism related genes in idiopathic pulmonary fibrosis and its correlation with immune microenvironment.Scientific reports · 2025Article
- Oral Lichen Planus: A Narrative Review Navigating Etiologies, Clinical Manifestations, Diagnostics, and Therapeutic Approaches.Journal of clinical medicine · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Oral lichen planus (OLP) is a type of chronic inflammatory disorder, which represents a potential risk of malignant transformation. Understanding the mechanism of OLP-related malignant transformation could reduce the risk of cancer. Accumulating evidence indicates that the expression of succinate dehydrogenase enzyme B (SDHB) is associated with the carcinogenesis of oral squamous cell carcinoma (OSCC). However, the function and underlying mechanism of SDHB in OLP remains unknown. Methods: In this study, we examined the expression of SDHB in tissues from OLP patients and normal oral mucosa (NOM) through immunohistochemical (IHC) staining, quantitative reverse transcription polymerase chain reaction (qRT-PCR), and western blot (WB). Adenosine triphosphate (ATP) assay, reactive oxygen species (ROS) assay, mitochondrial membrane potential (MMP) assay, and glucose uptake assay were used to explore the function of SDHB in mitochondrial injury and bioenergetic changes in OLP cell model and SDHB-overexpressing cells. Results: In current study, we found that the messenger RNA (mRNA) and protein expression of SDHB was significantly decreased in OLP patients, accompanied by the accumulation of succinate. In the lipopolysaccharide (LPS) or CoCl Conclusions: Our study suggests that SDHB reduction promotes OLP by impairing mitochondrial respiratory function.
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Registered trials
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