ArticleRespiratory research2024
Vitamin D ameliorates particulate matter induced mitochondrial damages and calcium dyshomeostasis in BEAS-2B human bronchial epithelial cells.
Article in Respiratory research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Endoplasmic reticulum stress-mediated disruption of mitochondrial homeostasis drives airway epithelial barrier fragility and enhances susceptibility to recurrent respiratory tract infections in children.Translational pediatrics · 2026Article
- Epithelial-immune interface in asthma: Mechanistic insights driving novel therapeutic strategies.Seminars in immunopathology · 2026Review
- Review
- Vitamin D in Cardiovascular Medicine: From Molecular Mechanisms to Clinical Translation.Nutrients · 2026Review
- A nonlinear, causal link between serum 25-hydroxyvitamin D and prolactin in type 2 diabetes: Evidence from clinical and Mendelian randomization analyses.Metabolism open · 2025Article
- Chronic obstructive pulmonary disease: in-depth analysis of microbiota association and innovative prevention and treatment approaches from the gut-lung axis perspective.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundMitochondria is prone to oxidative damage by endogenous and exogenous sources of free radicals, including particulate matter (PM). Given the role of mitochondria in inflammatory disorders, such as asthma and chronic obstructive pulmonary disease, we hypothesized that supplementation of vitamin D may play a protective role in PM-induced mitochondrial oxidative damages of human bronchial epithelial BEAS-2B cells.
methodsBEAS-2B cells were pretreated with 1,25(OH)
resultsOur findings first showed that 24-hour exposure to PM led to the overproduction of reactive oxygen species (ROS) derived from mitochondria. PM-induced mitochondrial oxidation resulted in intracellular calcium accumulation, particularly within mitochondria, and alterations in mitochondrial morphology and functions. These changes included loss of mitochondrial membrane integrity, disarrayed cristae, mitochondrial membrane depolarization, reduced ATP production, and increased mitochondrial DNA copy number. Consequently, PM-induced mitochondrial damage triggered the release of certain inflammatory cytokines, such as IL-6 and MCP-1. Similar to the actions of mitochondrial ROS inhibitor MitoTEMPO, 1,25(OH)
conclusionOur study provides new evidence that 1,25(OH)
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