ArticleClinical and translational medicine2021
Vitamin D3 ameliorates nitrogen mustard-induced cutaneous inflammation by inactivating the NLRP3 inflammasome through the SIRT3-SOD2-mtROS signaling pathway.
Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 60 citations in OpenAlex.
- Molecular Drivers of Cognitive Decline and Neuroprotection in Obstructive Sleep Apnea: A Narrative Review.Antioxidants (Basel, Switzerland) · 2026Review
- Nitrogen Mustard Disrupts Bioenergetics and Activates Oxidative Stress-Induced Cell Death Pathways in Human Keratinocytes.Chemical research in toxicology · 2026Article
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- Beyond bones, vitamin D as a sunshine hormone in type 2 diabetes mellitus and its complications.iScience · 2026Review
- The Interplay Among Gut Microbial Composition, Short-Chain Fatty Acid Metabolism and Gut-Kidney Oxidative Stress: Correlation with Diarrhea.Journal of inflammation research · 2026Article
- Metformin Inhibits Inflammation by Targeting the NLRP3 Inflammasome: Linking NF-κB/NEK7/AMPK Signaling to Mitochondrial Function.Journal of inflammation research · 2026Review
- Risk stratification in intermediate asymptomatic carotid artery disease: a multi-modal approach combining local flow dynamics and systemic clinical profiles.Frontiers in surgery · 2026Article
- Vitamin DFrontiers in immunology · 2026Review
- 1,25-Dihydroxyvitamin D3 ameliorates neutrophilic asthma through modulation of ERS-NLRP3 inflammasome axis in a mouse model.Iranian journal of basic medical sciences · 2026Article
- Targeting LINC00707 by vitamin D3 attenuates nitrogen mustard-caused dermal toxicity through inhibiting ferroptosis.Redox biology · 2025Article
- Vitamin D3 suppresses NLRP3 inflammasome pathway and enhances steroid sensitivity in a neutrophilic steroid hyporesponsive asthma mouse model.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Asiatic acid improves the damage of HaCaT cells induced by nitrogen mustard through inhibiting endoplasmic reticulum stress.Toxicology research · 2025Article
- STING-mediated neuroinflammation: a therapeutic target in neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- Nitrogen mustard induces dynamic nuclear protein spectrum change and DNA-protein crosslinking, with p97 mediating repair.Heliyon · 2024Article
- The NADase CD38 is a central regulator in gouty inflammation and a novel druggable therapeutic target.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Empagliflozin ameliorates vascular calcification in diabetic mice through inhibiting Bhlhe40-dependent NLRP3 inflammasome activation.Acta pharmacologica Sinica · 2024Article
- HSP90, a Common Therapeutic Target for Suppressing Skin Injury Caused by Exposure to Chemically Diverse Classes of Blistering Agents.The Journal of pharmacology and experimental therapeutics · 2024Article
- The Role of Histone Deacetylases in NLRP3 Inflammasomesmediated Epilepsy.Current molecular medicine · 2024Review
- Article
- New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases.Nutrients · 2023Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitrogen mustard (NM) causes severe skin injury with an obvious inflammatory response, which is lack of effective and targeted therapies. Vitamin D3 (VD3) has excellent anti-inflammatory properties and is considered as a potential candidate for the treatment of NM-induced dermal toxicity; however, the underlying mechanisms are currently unclear. Cyclooxygenase-2 (COX2; a widely used marker of skin inflammation) plays a key role in NM-induced cutaneous inflammation. Herein, we initially confirmed that NM markedly promoted COX2 expression in vitro and in vivo. NM also increased NOD-like receptor family pyrin domain containing 3 (NLRP3) expression, caspase-1 activity, and interleukin-1β (IL-1β) release. Notably, treatment with a caspase-1 inhibitor (zYVAD-fmk), NLRP3 inhibitor (MCC950), and NLRP3 or caspase-1 siRNA attenuated NM-induced NLRP3 inflammasome activation, with subsequent suppression of COX2 expression and IL-1β release in keratinocytes. Meanwhile, NM increased mitochondrial reactive oxygen species (mtROS) and decreased manganese superoxide dismutase 2 (SOD2) and sirtuin 3 (SIRT3) activities. Mito-TEMPO (a mtROS scavenger) ameliorated NM-caused NLRP3 inflammasome activation in keratinocytes. Moreover, VD3 improved SIRT3 and SOD2 activities, decreased mtROS contents, inactivated the NLRP3 inflammasome, and attenuated cutaneous inflammation induced by NM in vitro and in vivo. The beneficial activity of VD3 against NM-triggered cutaneous inflammation was enhanced by the inhibitors of IL-1, mtROS, NLRP3, caspase-1, and NLRP3 or caspase-1 siRNAs, which was abolished in SIRT3 inhibitor or SIRT3 siRNA-treated keratinocytes and skins from SIRT3
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