Identification of Critical Biomarkers and Mechanisms of Fructus Ligustri Lucidi on Vitiligo Using Integrated Bioinformatics Analysis DOI Creative Commons

Tian-Shan Liang,

Nan Tang, Minghua Xian

et al.

Clinical Cosmetic and Investigational Dermatology, Journal Year: 2023, Volume and Issue: Volume 16, P. 2061 - 2071

Published: Aug. 1, 2023

Vitiligo is an autoimmune disease of the skin that targets pigment-producing melanocytes and results in patches depigmentation are visible as white spots. Recent research studies have yielded a strong mechanistic understanding this disease. Fructus Ligustri Lucidi (FLL) has been used for premature graying hair since ancient China currently to treat vitiligo. However, key biomarkers mechanisms underlying FLL vitiligo remain unclear. This study aimed identify potential using network pharmacology analysis.The expression profiles GSE65127 GSE75819 were downloaded from Gene Expression Omnibus database differentially expressed genes (DEGs) between healthy samples. ontology Kyoto Encyclopedia Genes Genomes (KEGG) pathway enrichment DEGs performed R analyses. We further understand functions critical targets. Cytoscape tools facilitated topology analysis. Molecular docking was Auto Dock Vina software.The showed 13 screened Based on bioinformatics, Western blot, we found melanoma antigen recognized by 5,6-dihydroxyindole-2-carboxylic acid oxidase (TYRP1) may be related mechanism action treatment vitiligo.TYRP1, melanocyte molecular biomarker, closely via inhibition death.

Language: Английский

Hair Follicle Melanocytes Initiate Autoimmunity in Alopecia Areata: a Trigger Point DOI
Bo Xie, Jiayi Sun, Xiuzu Song

et al.

Clinical Reviews in Allergy & Immunology, Journal Year: 2022, Volume and Issue: 63(3), P. 417 - 430

Published: Sept. 19, 2022

Language: Английский

Citations

23
Treatment update for vitiligo based on autoimmune inhibition and melanocyte protection DOI
Bo Xie,

Yuqi Zhu,

Yuqing Shen

et al.

Expert Opinion on Therapeutic Targets, Journal Year: 2023, Volume and Issue: 27(3), P. 189 - 206

Published: March 4, 2023

Introduction The treatment of vitiligo remains challenging due to the complexity its pathogenesis, influenced by genetic factors, oxidative stress and abnormal cell adhesion that collectively impact melanocyte survival trigger immune system attacks, resulting in death. Melanocytes are believed exhibit susceptibility defects cellular mechanisms, such as autophagy, reduce their ability resist stress, leading increased expression pro-inflammatory protein HSP70. low molecules, DDR1 E-cadherin, accelerates damage antigen exposure. Consequently, autoimmune attacks centered on IFN-γ-CXCR9/10-CXCR3-CD8+ T cells initiated, causing vitiligo.

Language: Английский

Citations

12
Vitiligo: Etiology and Pathophysiology DOI Creative Commons
Rawan Almutairi

IntechOpen eBooks, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 6, 2025

Vitiligo’s etiology is still unclear and remains the subject of many studies. It considered to be an autoimmune-related disease in which autoantigens recognized by T cells from vitiligo patient were identified during last decades. Autoimmune reactions against melanocytes transfer specific antigens are required for development disease. In addition, environmental factors may involved vitiligo’s triggering or facilitating appearance lesions. Recently, oxidative stress has been as a modification microenvironment, several can promote inhibit terms treatments, since number conventional treatment techniques have established, therapy advanced significantly few years. Nevertheless, there currently no permanent vitiligo. necessitates determining signaling pathways target molecules particularly compromised This chapter intends address pathophysiology vitiligo, attempts new developments treatment, biologics Janus kinases (JAK) inhibitors.

Language: Английский

Citations

0
Bridging Molecular Mechanism and Clinical Practice in Vitiligo Treatment: An Updated Review DOI Creative Commons
Hyun Jeong Ju, Jung Min Bae

Dermatology, Journal Year: 2024, Volume and Issue: 240(3), P. 474 - 486

Published: Jan. 1, 2024

<b><i>Background:</i></b> Treatment of vitiligo seeks to achieve three goals: cessation disease progression, regeneration pigmentation, and prevention recurrence. <b><i>Summary:</i></b> Number nonsurgical interventions are available that suppress the autoimmune response regenerate melanocytes from reservoir: phototherapy including psoralen ultraviolet A, narrowband B, 308-nm excimer 311-nm Titanium:Sapphire lasers; topical agents calcineurin inhibitors, corticosteroids, 5-fluorouracil; systemic corticosteorids, mycophenolate mofetil, cyclosporine, methotrexate, minocycline, afamelanotide, antioxidants. In recent years, a great advance has been made in understanding pathogenesis vitiligo, JAK inhibitors being investigated as new treatment. Minimally invasive procedures such fractional lasers or microneedling can help optimal treatment outcome when used properly. <b><i>Key Messages:</i></b> Our review describes various modalities for based on their molecular mechanism action. Bridging gap between mechanisms therapeutic options would be valuable reference physicians clinical practice.

Language: Английский

Citations

3
The underestimated role of mitochondria in vitiligo: From oxidative stress to inflammation and cell death DOI Open Access
Yi Lin, Yuecen Ding, Yue Wu

et al.

Experimental Dermatology, Journal Year: 2023, Volume and Issue: 33(1)

Published: June 20, 2023

Abstract Vitiligo is an acquired depigmentary disorder characterized by the depletion of melanocytes in skin. Mitochondria shoulder multiple functions cells, such as production ATP, maintenance redox balance, initiation inflammation and regulation cell death. Increasing evidence has implicated involvement mitochondria pathogenesis vitiligo. alteration will cause abnormalities mentioned above, ultimately leading to melanocyte loss through various death modes. Nuclear factor erythroid 2‐related 2 (Nrf2) plays a critical role mitochondrial homeostasis, downregulation Nrf2 vitiligo may correlate with damage, making both promising targets treatment In this review, we aim discuss alterations its

Language: Английский

Citations

9
Abnormal metabolism in melanocytes participates in the activation of dendritic cell in halo nevus DOI

Ling Jiang,

Yibo Hu,

Yushan Zhang

et al.

Clinical Immunology, Journal Year: 2024, Volume and Issue: 265, P. 110300 - 110300

Published: June 29, 2024

Language: Английский

Citations

2
Differential Expression of Serum Exosomal Hsa-miR-487b-3p in Progressive Vitiligo Before and After Systemic Corticosteroid Treatment DOI Creative Commons

Haixin Luo,

Bo Xie, Jinhui Xu

et al.

Clinical Cosmetic and Investigational Dermatology, Journal Year: 2022, Volume and Issue: Volume 15, P. 1377 - 1386

Published: July 1, 2022

Vitiligo is an acquired skin depigmentation disease. It can be misdiagnosed at early stage and tend to relapse. Serum markers are essential monitoring the progression of vitiligo. Exosomal miRNAs act as communication mediator between melanocytes immune cells. Our study aimed use serum exosomal a reference for evaluating vitiligo progression.

Language: Английский

Citations

8
Mechanisms of autophagy and their implications in dermatological disorders DOI Creative Commons
Shibei Xue,

Yumeng Lin,

Haoran Chen

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Nov. 4, 2024

Autophagy is a highly conserved cellular self-digestive process that underlies the maintenance of homeostasis. classified into three types: macrophage, chaperone-mediated autophagy (CMA) and microphagy, which maintain homeostasis through different mechanisms. Altered regulation affects progression various skin diseases, including psoriasis (PA), systemic lupus erythematosus (SLE), vitiligo, atopic dermatitis (AD), alopecia areata (AA) sclerosis (SSc). In this review, we review existing literature focusing on mechanisms autophagy, namely as well roles in above six dermatological disorders order to aid further studies future.

Language: Английский

Citations

1
Targets Exploration of Hydroxychloroquine for Pigmentation and Cell Protection Effect in Melanocytes: The Clue for Vitiligo Treatment DOI Creative Commons
Bo Xie, Yi Chen, Yebei Hu

et al.

Drug Design Development and Therapy, Journal Year: 2022, Volume and Issue: Volume 16, P. 1011 - 1024

Published: April 1, 2022

The treatment of vitiligo is often challenging to dermatologists. There ample evidence suggest that hydroxychloroquine (HCQ) effective for treatment; nonetheless, the underlying mechanism remains unknown. In present study, we sought uncover molecular targets HCQ by an integrated network-based pharmacologic and transcriptomic approach.The potential were retrieved from databases based on crystal structure. Targets related screened intersected with HCQ. A protein-protein interaction network was generated. Interactions between verified docking. Moreover, human immortalized melanocytes (PIG3V) evaluated after (1μg/mL) 24h. total RNA PIG3V extracted determined RNA-seq transcriptomics differential gene expression analysis. Network pharmacology then used identify relationships putative differentially expressed genes.Molecular docking analysis revealed four key (ACHE, PNMT, MC1R, VDR) played important roles in treatment. According results, melanosomal biogenesis-related BLOC1S5 upregulated 138005.020 fold Genes protein repair (MSRB3) anti-ultraviolet (UV) effect (UVSSA) 4.253 2.603 fold, respectively, treatment.The significantly upregulated, indicating biogenesis addition, yields a protective upregulating genes associated damaged anti-UV (UVSSA). effects are mediated binding ACHE, VDR according verification.

Language: Английский

Citations

4
Transient receptor potential mucolipin 1 circumvents oxidative stress in primary human melanocytes DOI Creative Commons
Yi Chen, Bo Xie, Yebei Hu

et al.

Skin Research and Technology, Journal Year: 2024, Volume and Issue: 30(6)

Published: June 1, 2024

Abstract Background Transient Receptor Potential Mucolipin 1 (TRPML1) serves as a pivotal reactive oxygen species (ROS) sensor in cells, which is implicated the regulation of autophagy. However, its function melanocyte autophagy under oxidative stress remains elusive. Methods The expression and ion channel TRPML1 were investigated using immunofluorescence calcium imaging primary human melanocytes (MCs). After activating with MLSA1 (TRPML1 agonist), autophagy‐related molecules via western blot. ROS level, apoptosis‐ after pretreatment MLSA1. interference expression, mitochondrial structures visualized by electron microscopy hydrogen peroxide (H 2 O ）treatment. Results was expressed functionally active MCs, activation promotes elevated LC3‐II reduced apoptosis levels stress. downregulation caused swelling disruption cristae MCs. Conclusions might mediate lysosomal MCs stress, participating mechanisms that maintain antioxidant systems balance.

Language: Английский

Citations

0