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Xingyue Gao,1 Sihao Shen,1 Wenzhong Xiang,2 Xiuzu Song2 1The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou Third People’s Hospital, Hangzhou, People’s Republic of China; 2Department of Dermatology, Hangzhou Third People’s Hospital, Hangzhou, People’s Republic of ChinaCorrespondence: Wenzhong Xiang, Department of Dermatology, Hangzhou Third People’s Hospital, Westlake Ave 38, Hangzhou, 310002, People’s Republic of China, Email xiangwenzhong@126.comPurpose: Coronavirus disease (COVID-19) may trigger the reactivation of the latent varicella-zoster virus and may be a risk factor for herpes zoster (HZ). However, the causal relationship between COVID-19 and varicella-zoster infections remains controversial. This study aimed to estimate the causal inferences between COVID-19 and HZ.Methods: This study used a two-sample Mendelian randomization (MR) design. The inverse variance-weighted method was used as the primary method and sensitivity analyses were conducted, including the MR-Egger regression, weighted median and weighted mode. We searched at https://gwas.mrcieu.ac.uk/ using the keywords “COVID-19” for exposure data and “zoster” for outcome datasets.Results: We got 26 COVID-19 datasets and five zoster datasets. We used 26 COVID-19 datasets as exposure data corresponding to each zoster dataset for the MR analysis. There were nine datasets of COVID-19 where the number of SNPs was fewer than three in the MR analysis of the risk of HZ, varicella zoster virus (VZV) glycoprotein E and I antibody levels, anti-VZV IgG seropositivity, and post-zoster neuralgia. In addition, there were 10 datasets of COVID-19 where the number of SNPs was less than three in the MR analysis of anti-VZV IgG levels. The results of the MR analysis showed that all p-values were greater than 0.05. Sensitivity analysis revealed no evidence of horizontal pleiotropy in most two sample MR analyses.Conclusion: Our results indicate that there is no causa

Xiaofan Jin,1 Xiuzu Song2 1Zhejiang University School of Medicine, Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Hangzhou, People’s Republic of China; 2Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of ChinaCorrespondence: Xiuzu Song, Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, Westlake Ave 38, Hangzhou, 310009, People’s Republic of China, Email songxiuzu@sina.comAbstract: Autophagy is recognized as a crucial regulatory process, instrumental in the removal of senescent, dysfunctional, and damaged cells. Within the autophagic process, lysosomal digestion plays a critical role in the elimination of impaired organelles, thus preserving fundamental cellular metabolic functions and various biological processes. Mitophagy, a targeted autophagic process that specifically focuses on mitochondria, is essential for sustaining cellular health and energy balance. Therefore, a deep comprehension of the operational mechanisms and implications of autophagy and mitophagy is vital for disease prevention and treatment. In this context, we examine the role of autophagy and mitophagy during hair follicle cycles, closely scrutinizing their potential association with hair loss. We also conduct a thorough review of the regulatory mechanisms behind autophagy and mitophagy, highlighting their interaction with hair follicle stem cells and dermal papilla cells. In conclusion, we investigate the potential of manipulating autophagy and mitophagy pathways to develop innovative therapeutic strategies for hair loss.Keywords: hair follicle, mitophagy, dermal papilla cell, hair follicle stem cell, alopecia

Yuqing Shen,1 Yuqi Zhu,1 Li Zhang,1 Jiayi Sun,1 Bo Xie,2 Hongyan Zhang,2 Xiuzu Song2 1Department of Dermatology, Hangzhou Third People’s Hospital, Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China; 2Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital of Zhejiang University School of Medicine, Hangzhou, People’s Republic of ChinaCorrespondence: Xiuzu Song, Hangzhou Third People’s Hospital, Hangzhou, People’s Republic of China, Email songxiuzu@sina.comObjective: To investigate the mechanism of minoxidil in treating androgenetic alopecia (AGA).Methods: The mechanism of action of minoxidil on AGA was first systematically investigated from the viewpoint of network pharmacology, including minoxidil-AGA target prediction, protein-protein interaction (PPI) network analysis, molecular docking and enrichment analysis of targets related to minoxidil and AGA, and dermal papilla cell assays to confirm the viability of prediction.Results: The combined analysis revealed that minoxidil treatment of AGA not only acts on androgenic receptors (AR) but also on 2 new targets, steroid 17-alpha-hydroxylase/17,20 lyase (CYP17A1) and aromatase (CYP19A1). The biological processes linked to these targets were concentrated on several pathways, including enzymes and hormones. Further experiments have revealed that minoxidil suppresses the expression of AR and CYP17A1, boosts the activity of CYP19A1, decreases the formation and binding of dihydrotestosterone, and enhances the production of estradiol. Through these changes, minoxidil acts as a treatment for AGA.Conclusion: Minoxidil may act by altering hormonal and enzymatic pathways. Our study finds two new targets (CYP17A1, CYP19A1) of minoxidil and demonstrates that minoxidil inhibits AR. These targets may provide new ideas for drug research.Keywords: minoxidil, androgenetic alopecia, targets

Qingwei Geng,1,* Guoqi Wei,2,* Yebei Hu,1 Jinhui Xu,1 Xiuzu Song1 1Department of Dermatology, Hangzhou Third People’s Hospital, Hangzhou, Zhejiang, 310009, People’s Republic of China; 2Hangzhou Fuyang Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang, 322499, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiuzu Song, Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, West Lake Road 38, Hangzhou, 310009, People’s Republic of China, Tel +86-0571-87823102, Email songxiuzu@sina.comBackground: The skin barrier is the first line of defense of the body, while skin lipids play an important role in the skin permeability barrier. Lamellar bodies are also involved in maintaining the stability of the skin permeability barrier. However, the exact origin of lamellar bodies remains unclear. Recent studies have suggested that autophagy may participate in the formation of lamellar bodies.Aim: This study aimed to investigate the role of autophagy in the formation of lamellar bodies in keratinocytes and the regulation of keratinocyte lipids.Methods: Keratinocytes were incubated with autophagy inducer Rapamycin and autophagy inhibitor Bafilomycin A1. The changes in autophagy flux were detected by Western blot, and the formation of lamellar bodies was observed by transmission electron microscopy. Furthermore, the changes in keratinocytes lipidomics were detected by liquid chromatography-mass spectrometry.Results: Our research showed that the autophagy inducer promoted autophagy activation and formation of lamellar bodies in keratinocytes, while the inhibitor inhibited autophagy signals and the formation of lamellar bodies in keratinocytes. In addition, the lipidomics results revealed a significant change in glycerophospholipids after autophagy induction and autophagy inhibition.Conclusion: These results demonst

Haixin Luo,1,* Bo Xie,2,* Jinhui Xu,2 Yuqi Zhu,1 Jiayi Sun,1 Yuqing Shen,1 Xiuzu Song2 1Department of Dermatology, Hangzhou Third Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, People’s Republic of China; 2Department of Dermatology, Hangzhou Third People’s Hospital; Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, Hangzhou, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiuzu Song, Email songxiuzu@sina.comBackground: Vitiligo is an acquired skin depigmentation disease. It can be misdiagnosed at an early stage and tend to relapse. Serum markers are essential to monitoring the progression of vitiligo. Exosomal miRNAs act as the communication mediator between melanocytes and immune cells. Our study aimed to use serum exosomal miRNAs as a reference for evaluating vitiligo progression.Methods: The miRNAs were extracted from the serum exosomes of ten progressive vitiligo patients (before and after treatment) and ten healthy individuals. We profiled miRNAs expression by RNA sequencing and screened out potential miRNAs and plotted their receiver operating characteristic (ROC) curves to explore their sensitivity and specificity as prognostic biomarkers in vitiligo progression. We examined the correlation between miRNA expression and the lesion area. Different databases were used to predict gene targets of miRNAs, which were analyzed by gene ontology and Kyoto encyclopedia of genes and genomes (KEGG).Results: Our results showed that 141 miRNAs were differentially expressed in serum exosomes of progressive vitiligo patients, and 365 miRNAs were differentially expressed in these patients after treatment compared to healthy individuals. The expression of hsa-miR-487b-3p was significantly lower in these patients compared to healthy individuals. Still, there was no difference in its levels in patients after corticosteroid treatment compared to healthy con

Bo Xie,1,* Yi Chen,2,* Yebei Hu,2 Yan Zhao,2 Haixin Luo,2 Jinhui Xu,1 Xiuzu Song1 1Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, Hangzhou, 310009, People’s Republic of China; 2Department of Dermatology, Hangzhou Third Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, 310009, People’s Republic of China*These authors contributed equally to this workCorrespondence: Xiuzu Song, Department of Dermatology, Hangzhou Third People’s Hospital, Affiliated Hangzhou Dermatology Hospital, Zhejiang University School of Medicine, West Lake Road 38, Hangzhou, 310009, People’s Republic of China, Tel +86-571-87823102, Email songxiuzu@sina.comObjective: The treatment of vitiligo is often challenging to dermatologists. There is ample evidence to suggest that hydroxychloroquine (HCQ) is effective for vitiligo treatment; nonetheless, the underlying mechanism remains unknown. In the present study, we sought to uncover the molecular targets of HCQ by an integrated network-based pharmacologic and transcriptomic approach.Methods: The potential targets of HCQ were retrieved from databases based on the crystal structure. Targets related to vitiligo were screened and intersected with potential targets of HCQ. A protein-protein interaction network of the intersected targets was generated. Interactions between the targets were verified by molecular docking. Moreover, human vitiligo immortalized melanocytes (PIG3V) were evaluated after treatment with HCQ (1μg/mL) for 24h. The total RNA of PIG3V was extracted and determined by RNA-seq transcriptomics for differential gene expression analysis. Network pharmacology was then used to identify the relationships between putative targets of HCQ and differentially expressed genes.Results: Molecular docking analysis revealed four putative key targets (ACHE, PNMT, MC1R, and VDR) of HCQ played important roles i