ArticleFrontiers in cell and developmental biology2020
Tranilast Directly Targets NLRP3 to Protect Melanocytes From Keratinocyte-Derived IL-1β Under Oxidative Stress.
Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 35 citations in OpenAlex.
- The challenge of cell death switching in inflammasome-targeted therapies for bacterial and viral infections.Communications biology · 2026Review
- Vitiligo as a Failure of Immune Resolution and Tissue Regeneration: From Stress Signals to Targeted Immune Modulation.Clinical reviews in allergy & immunology · 2026Review
- Tranilast ameliorates experimental abdominal aortic aneurysm by inhibiting the NLRP3 inflammasome pathway.Journal of pharmaceutical analysis · 2026Article
- TKI-mediated inhibition of NLRP1 inflammasome restores erythropoiesis in DBA syndrome.EMBO molecular medicine · 2026Article
- Neuroinflammation in Alzheimer's disease-associated sensory dysfunction: mechanistic links, actionable targets and therapeutic strategies.Frontiers in aging neuroscience · 2026Review
- Neuroimmune Dysregulation and AI-Driven Therapeutic Strategies in Alzheimer's Disease.Cellular and molecular neurobiology · 2025Review
- A Scoping Review of Pathogenesis, Current Treatments, and Novel Approaches for Vitiligo.Journal of cosmetic dermatology · 2025Article
- Mechanisms of Resistance to Anti-PD-1 Immunotherapy in Melanoma and Strategies to Overcome It.Biomolecules · 2025Review
- Review
- Novel antimicrobial peptides against Cutibacterium acnes designed by deep learning.Scientific reports · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Targeting NLRP3 Inflammasome: Structure, Function, and Inhibitors.Current medicinal chemistry · 2024Article
- Tranilast reduces cardiomyocyte injury induced by ischemia‑reperfusion via Nrf2/HO‑1/NF‑κB signaling.Experimental and therapeutic medicine · 2023Article
- Reversing Gray Hair: Inspiring the Development of New Therapies Through Research on Hair Pigmentation and Repigmentation Progress.International journal of biological sciences · 2023Review
- Insights into the Role of Inflammation in the Management of Atherosclerosis.Journal of inflammation research · 2023Review
- The Current Status of Antioxidants in the Treatment of Vitiligo in China.Oxidative medicine and cellular longevity · 2022Article
- Mechanisms of Immunotherapy Resistance in Cutaneous Melanoma: Recognizing a Shapeshifter.Frontiers in oncology · 2022Review
- The NLRP3 Inflammasome Pathway: A Review of Mechanisms and Inhibitors for the Treatment of Inflammatory Diseases.Frontiers in aging neuroscience · 2022Review
- The Promising Role of Chemokines in Vitiligo: From Oxidative Stress to the Autoimmune Response.Oxidative medicine and cellular longevity · 2022Review
- Tranilast inhibits angiotensin II-induced myocardial fibrosis through S100A11/ transforming growth factor-β (TGF-β1)/Smad axis.Bioengineered · 2021Article
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of NLRP3 inflammasome-IL-1β pathway in keratinocytes contributes to the melanocyte death via autoimmunity-dependent manner in vitiligo. As a safe small-compound drug employed frequently in clinic, tranilast (TR) is newly reported to block the activation of NLRP3 inflammasome in macrophage. Nevertheless, whether keratinocyte-derived IL-1β damages melanocytes in an autoimmunity-independent way and whether TR could ameliorate the melanocyte damage via inhibiting the NLRP3-IL-1β pathway in keratinocyte still are not clear. In the present study, we initially found that TR could impede the secretion of IL-1β from keratinocytes by interfering the NLRP3 oligomerization. More importantly, we illustrated that TR could decrease the melanocyte apoptosis, improve the melanogenesis, and have the capacity to optimize the melanosome translocation by abolishing the keratinocyte-derived IL-1β. Additionally, TR could mitigate the secretion of inflammatory cytokines such as IL-6, IL-8, TNF-α, and IL-18 in keratinocytes under oxidative stress. In short, our data indicate that IL-1β plays detrimental roles in the melanocyte survival, melanogenesis, melanosome translocation and the secretion of inflammatory cytokines, and TR could be a promising therapeutic strategy in vitiligo by attenuating the keratinocyte-derived IL-1β under oxidative stress.
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