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This article explores the potential causal relationship between obesity and rosacea, a chronic inflammatory skin disorder. Using Mendelian randomization analysis, the study found no association between genetic susceptibility to obesity and the risk of rosacea. The authors suggest that previous observational studies may have limitations in determining causality and associations due to measurement errors and population differences. Further research is needed to confirm these findings in other races and rosacea subtypes and regions. The study was supported by funding from the Hangzhou Biomedical and Health Industry Development Support Project and the Hangzhou Medical Key Discipline Construction Project, and the authors declare no conflicts of interest. [Extracted from the article]

This study aimed to investigate the protective effect of NAcM‐OPT, a small molecule inhibitor of defective in cullin neddylation 1 (DCN1), on H2O2‐induced oxidative damage in keratinocytes. Immortalized human keratinocytes (HaCaT cells) were treated with NAcM‐OPT and exposed to oxidative stress. CCK‐8 assays were used to measure cell viability. The mGFP‐RFP‐LC3 dual fluorescent autophagy indicator system was utilized to evaluate changes in autophagic flux. Western blotting was used to measure the expression of the autophagy‐related proteins LC3 and Beclin 1. Keratinocytes were treated with the autophagy activator rapamycin, and HaCaT cell supernatant was added to PIG1 cells (immortalized human melanocytes), followed by evaluation of tyrosinase (TYR) expression via qRT‐PCR. NAcM‐OPT increased cell viability and cell proliferation. Furthermore, this molecule promoted autophagic flux through increased expression of autophagy‐related proteins under H2O2‐induced oxidative stress. Additionally, rapamycin increased the mRNA levels of TYR in PIG1 cells. Moreover, NAcM‐OPT alleviated mitochondrial damage, restored mitochondrial function, and upregulated the expression of NFE2L2, HO1, NQO1, and GCLM. Importantly, NAcM‐OPT also increased epidermal thickness, follicle length, and melanin synthesis under oxidative stress in vivo. These findings suggest that NAcM‐OPT may be a promising small molecule antioxidant drug for the treatment of vitiligo. [ABSTRACT FROM AUTHOR]

Purpose: 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 causal relationship between COVID-19 and varicella-zoster infection, HZ progression, and postherpetic neuralgia. [ABSTRACT FROM AUTHOR]

Background: An increasing amount of research demonstrates that metabolic disorders are related to rosacea. However, the correlations and causal relationships among them remain unknown. Methods: We conducted not only forward 2‐sample MR (Mendelian randomization) analyses but also reverse MR analyses which showed positive results in the forward MR analysis. In the forward MR analyses, inverse‐variance weighted (IVW) and MR‐Egger were performed as MR analyses. Cochran's Q test and the MR‐Egger Intercept were used for sensitivity analyses. Concerning reverse MR analyses, IVW, MR‐Egger, weighted median, simple mode, and weighted mode were applied. Cochran's Q test, MR‐Egger Intercept, and MR pleiotropy residual sum and outlier (MR‐PRESSO) outlier test were applied as sensitivity analyses. Results: A total of 24 metabolites and 1 metabolite ratio were shown to have a causal effect on rosacea. N‐lactoyl phenylalanine (N‐Lac‐Phe) was estimated as statistically significant by Bonferroni correction. Interestingly, we found three metabolites that were negatively associated with rosacea, especially caffeine, which are in line with the results of a large cohort study of females. For reverse MR analysis, we revealed that rosacea could potentially decrease the generation of two metabolites: octadecenedioate (C18:1−DC) and methyl vanillate sulfate. Conclusion: This study identified blood metabolites that may be associated with the development of rosacea. However, the exact mechanism by which these positive metabolites influence rosacea remains uncertain due to the paucity of experimental investigations. The combination of genetics and metabolomics offers novel viewpoints on the research of underlying mechanisms of rosacea and has significant value in screening and prevention of rosacea. [ABSTRACT FROM AUTHOR]

Background: Ultraviolet (UV)‐induced fluorescence technology is widely used in dermatology to identify microbial infections. Our clinical observations under an ultraviolet‐induced fluorescent dermatoscope (UVFD) showed red fluorescence on the scalps of androgenetic alopecia (AGA) patients. In this study, based on the hypothesis that microbes are induced to emit red fluorescence under UV light, we aimed to explore the microbial disparities between the AGA fluorescent area (AF group) and AGA non‐fluorescent area (ANF group). Methods: Scalp swab samples were collected from 36 AGA patients, including both fluorescent and non‐fluorescent areas. The bacterial communities on the scalp were analyzed by 16S rRNA gene sequencing and bioinformatics analysis, as well as through microbial culture methods. Results: Significant variations were observed in microbial evenness, abundance composition, and functional predictions between fluorescent and non‐fluorescent areas. Sequencing results highlighted significant differences in Cutibacterium abundance between these areas (34.06% and 21.36%, respectively; p < 0.05). Furthermore, cultured red fluorescent colonies primarily consisted of Cutibacterium spp., Cutibacterium acnes, Staphylococcus epidermidis, and Micrococcus spp. Conclusions: This is the first study to investigate scalp red fluorescence, highlighting microbial composition variability across different scalp regions. These findings may provide novel insights into the microbiological mechanisms of AGA. [ABSTRACT FROM AUTHOR]

Background: Transient Receptor Potential Mucolipin 1 (TRPML1) serves as a pivotal reactive oxygen species (ROS) sensor in cells, which is implicated in the regulation of autophagy. However, its function in melanocyte autophagy under oxidative stress remains elusive. Methods: The expression and ion channel function of TRPML1 were investigated using immunofluorescence and calcium imaging in primary human melanocytes (MCs). After activating TRPML1 with MLSA1 (TRPML1 agonist), autophagy‐related molecules were investigated via western blot. ROS level, apoptosis‐ and autophagy‐related molecules were investigated after pretreatment with MLSA1. After interference with TRPML1 expression, mitochondrial structures were visualized by electron microscopy with hydrogen peroxide (H2O2）treatment. Results: TRPML1 was expressed and functionally active in primary human MCs, and its activation promotes elevated expression of LC3‐II and reduced apoptosis and ROS levels under oxidative stress. TRPML1 downregulation caused mitochondrial swelling and disruption of cristae structures under oxidative stress in primary human MCs. Conclusions: TRPML1 might mediate lysosomal autophagy in primary human MCs under oxidative stress, participating in mechanisms that maintain the oxidative and antioxidant systems in balance. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]