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Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders

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A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 8998

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Special Issue Editor

Dr. Xuming Zhu

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Guest Editor

1. Black Family Stem Cell Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
2. Institute for Regenerative Medicine, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
3. Department of Cell, Developmental and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
Interests: developmental biology; cutaneous biology; stem cell; epigenetic regulation; dry eye disease

Special Issue Information

Dear Colleagues,

The skin and its appendages, including hair follicles and exocrine glands, are intricate organs that require precise molecular regulation for proper development, homeostasis, and repair. Dysregulation in these processes can lead to a wide range of disorders, from common dermatological conditions such as psoriasis, atopic dermatitis, acne, and alopecia to more severe malignancies like melanoma and squamous cell carcinoma. This Special Issue, "Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders", aims to explore the underlying mechanisms and emerging therapeutic strategies for these conditions, bridging the gap between fundamental research and clinical translation.

Key topics include, but are not limited to, the following:

Developmental and homeostatic mechanisms;
Disease drivers in psoriasis, atopic dermatitis, acne, alopecia, and cutaneous cancers;
Innovative therapies, such as small-molecule inhibitors, biologics, and regenerative approaches;
Genetic and epigenetic factors in skin disorders.

We invite contributions that explore the molecular mechanisms regulating skin and appendage development, homeostasis, and tumorigenesis. By integrating multidisciplinary approaches, we aim to advance our understanding of these complex processes and improve therapeutic outcomes for patients. This Special Issue provides a platform for researchers and clinicians to share their latest findings and innovative strategies, fostering a collaborative environment dedicated to advancing the field of dermatology and cutaneous biology.

Dr. Xuming Zhu
Guest Editor

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Keywords

skin disorders
skin development
skin pathophysiology
tumorigenesis
psoriasis
atopic dermatitis
acne
innovative therapies
molecular dermatology
translational skin research

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Published Papers (7 papers)

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Research

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12 pages, 1575 KB

Open AccessArticle

Comparison of Quantitative Evaluation and Conventional Scar Scale Analysis for Pediatric Pathological Scars

by Jin-Ye Guan, Xing Zou, Jun-Wen Ge, Rui-Cheng Tian, Wei Liu, Mei-Yun Li and Dan Deng

Biomedicines 2026, 14(4), 784; https://doi.org/10.3390/biomedicines14040784 - 30 Mar 2026

Viewed by 542

Abstract

Background/Objectives: The incidence of pediatric pathological scars (PPS) has been gradually increasing due to various causes, highlighting the need for accurate scar assessment to monitor disease progression and therapeutic efficacy. Vancouver Scar Scale (VSS) and other scar evaluation systems are relatively subjective evaluation methods that rely on physicians’ or patients’ own judgment. By contrast, when comparing different scar scale evaluation methods, a three-dimensional (3D) camera and dermoscopy may provide relatively objective measurable parameters to avoid possible subjective bias created by the observers. This study aimed to compare the utility of traditional VSS evaluation with that of 3D cameras and dermoscopy in PPS evaluation. Methods: A total of 35 pediatric patients (aged 0–18 years) with PPS were involved, and their scars were assessed via the VSS, dermoscopy, and the Antera 3D^® system. In addition, a subset of 18 patients (36 scar regions) was also evaluated for therapeutic efficacy after 3–6 months of treatment. Briefly, VSS scores were blindly evaluated by two independent dermatologists under standardized conditions. Quantitative assessment was also performed using dermoscopy and the Antera 3D^® system. The former quantified chromatic parameters (pigmentation: L*, vascularity: a*, green value); the latter captured multispectral 3D images to analyze volume, pigmentation, and erythema. Data are presented as means ± standard deviation and analyzed using paired-sample t tests (one-tailed), the Wilcoxon signed-rank test, and standardized response means (SRMs) to assess therapeutic sensitivity, while baseline variability was evaluated using the standard deviation and coefficient of variation (CV). Results: The results showed that Antera 3D^® detected significant reductions in pigmentation (p < 0.01, SRM = −0.46), vascularity (p < 0.001, SRM = −0.59), and volume (p < 0.0001, SRM = −0.83), while dermoscopy indicated similar moderate improvements in vascularity (Green value: p < 0.001, SRM = 0.57; a*: p < 0.0001, SRM = −0.68) and pigmentation (L*: p < 0.0001, SRM = 0.48) after treatments. VSS showed significant gains in pliability (p < 0.0001, SRM = −1.13), height (p < 0.01, SRM = −0.54), and overall impression (p < 0.0001, SRM = −0.86), but minimal changes in pigmentation (p > 0.05, SRM = 0) or vascularity (p > 0.05, SRM = −0.21). At baseline, Antera 3D^® showed the greatest variability in pigmentation (CV 43.41%) and volume (CV 91.21%), followed by VSS in vascularity (CV 52.95%), pliability (CV 34.05%), and overall impression (CV 31.76%). Dermoscopy presented the lowest variability, indicating limited discriminative power. Conclusions: In conclusion, Antera 3D^® offers an objective, sensitive, and spatially precise approach for PPS assessment and may provide additional quantitative information for evaluating subtle and early changes alongside traditional scar assessment scales. Its integration into clinical practice will enhance treatment monitoring and support more accurate timing of therapeutic interventions. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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23 pages, 13995 KB

Open AccessArticle

Adalimumab Treatment Modulates Vascular Changes in Hidradenitis Suppurativa Lesions in a Sex-Dependent Manner

by Bepa Pavlić, Marin Ogorevc, Nela Kelam, Ana Stipić, Ema Borovina, Petar Hučić, Ante Čizmić, Dubravka Vuković, Katarina Vukojević, Mirna Saraga-Babić and Snježana Mardešić

Biomedicines 2026, 14(4), 741; https://doi.org/10.3390/biomedicines14040741 - 24 Mar 2026

Viewed by 535

Abstract

Background/Objectives: Hidradenitis suppurativa (HS) is a chronic, immune-mediated inflammatory skin disease characterized by painful nodules, abscesses, sinus tracts, and progressive fibrosis. Vascular activation is becoming increasingly acknowledged as an important factor in HS pathogenesis; however, the effects of tumor necrosis factor alpha (TNF-α) blockade on vascular remodeling in HS remain poorly characterized. This study investigated the impact of TNF-α inhibition by adalimumab (ADA) on endothelial and fibroblast-associated markers in HS lesions. Methods: Formalin-fixed paraffin-embedded skin samples from 71 HS patients were analyzed, including treatment-naive (n = 38) and adalimumab-treated (n = 33) cases. Histopathology and immunofluorescence were performed using antibodies against CD31, von Willebrand factor (vWF), α-smooth muscle actin (αSMA), vimentin, Ki-67 (proliferation), and cleaved Caspase-3 (apoptosis). ImageJ software was used to determine the immunoexpression of selected markers and vascular density. Vascular density, assessed as vessel count per mm², was designated as the primary endpoint. Sex-related differences were analyzed as exploratory endpoints. Results: Adalimumab-treated tissue exhibited significantly reduced vascular density (p < 0.01) compared to the treatment-naive group. Conversely, vimentin immunoexpression was significantly higher (p < 0.01) in the adalimumab-treated group. No significant differences were found in endothelial Ki-67 or cleaved Caspase-3 expression between treatment groups, indicating that the observed reduction in vascular density is not associated with direct effects on endothelial cell proliferation or apoptosis, but rather may occur indirectly through attenuation of the pro-angiogenic inflammatory milieu. Exploratory sex-stratified analysis revealed that treatment-naive males had significantly higher endothelial proliferation (Ki-67; p = 0.031) and vimentin expression (p = 0.017) compared to treatment-naive females. In the ADA-treated group, males exhibited significantly lower vascular density (p = 0.036) and higher endothelial apoptosis (p = 0.039) compared to females, whereas females showed a significant increase in vimentin expression following treatment (p = 0.008), suggesting possible sex-dependent differences in vascular remodeling. Conclusions: TNF-α blockade is associated with reduced vascular density, consistent with indirect anti-angiogenic effects, suggesting that adalimumab exerts disease-modifying effects on the microenvironment beyond inflammatory cytokine suppression. Sex-dependent differences in vascular regression underscore the importance of considering sex as a biological variable in HS pathogenesis and treatment response. These results highlight the significance of vascular interactions in HS and support adalimumab as a disease-modifying treatment. These exploratory findings require confirmation in longitudinal studies with paired biopsies. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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17 pages, 2917 KB

Open AccessArticle

Terminalia chebula Retz. Fruit Extract Promotes Murine Hair Growth by Suppressing 5α-Reductase and Accelerating the Degradation of Dihydrotestosterone

by Ting Cui, Xiaoqing Wang, Qi Wu, Ye Zhong, Fenglou Wang, Yue Zou, Yushu Wang, Shanshan Jiang and Gang Ma

Biomedicines 2025, 13(11), 2584; https://doi.org/10.3390/biomedicines13112584 - 22 Oct 2025

Cited by 2 | Viewed by 2337

Abstract

Background/Objectives: Androgenetic alopecia (AGA) is the most common hair loss disorder in dermatological practice. Its primary pathogenesis involves the conversion of testosterone to dihydrotestosterone (DHT) by type II 5α-reductase upon reaching dermal papilla cells (DPCs). DHT impairs DPCs’ activity and inhibits hair growth. Although the FDA-approved drugs finasteride and minoxidil show certain efficacy, they are also associated with severe side effects. This study aims to explore the effects of Terminalia chebula fruit extract (TCFE) on hair growth and its underlying molecular mechanisms. Methods: We investigated the therapeutic potential of TCFE in hair follicle regeneration, employing a multi-level experimental approach combining in vitro analyses of DPCs, in vivo animal models of AGA, and ex vivo cultures of human hair follicles and scalp tissue. Results: First, RNA-seq analysis and RT-PCR validation revealed that TCFE treatment activated the Wnt and TGF-β3 signaling pathways in DPCs, particularly upregulating the AKR1C gene family, which is involved in DHT metabolism. TCFE also potently inhibited type II 5α-reductase activity and mitigated DHT-induced damage to DPCs. In an AGA mouse model, TCFE reversed the AGA phenotype with efficacy comparable to finasteride. However, unlike finasteride, TCFE specifically enhanced the expression of AKR1C1 and AKR1C3, indicating a distinct mechanism. Finally, in ex vivo organ cultures, TCFE suppressed hair follicle cell apoptosis, promoted proliferation, and thereby stimulated hair growth. Conclusions: These findings suggest that TCFE is a promising natural treatment for AGA, likely acting through multiple mechanisms, including Wnt pathway activation, 5α-reductase inhibition, and enhanced DHT degradation. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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21 pages, 1078 KB

Open AccessArticle

Potential Risk of Cutaneous Melanoma Attributable to Medication Use: A Mendelian Randomization Approach

by Huiying Wan, Ling Zhong, Jia Su, Qiaofeng Zhao, Mitsutoshi Tominaga, Kenji Takamori, Hang Ma, Tian Xia and Dingding Zhang

Biomedicines 2025, 13(10), 2477; https://doi.org/10.3390/biomedicines13102477 - 11 Oct 2025

Viewed by 1109

Abstract

Background/Objective: Cutaneous melanoma is a highly heterogeneous malignancy and life-threatening skin cancer with rising global incidence. Although various therapeutic options are available, their clinical efficacy remains limited, highlighting the urgent need for novel strategies that facilitate prevention, diagnosis, and treatment. The aim of this study was to explore the potential causal association between medication use and the risk of developing cutaneous melanomas. Methods: Using summary data from Genome-Wide Association Studies (GWASs), we performed Mendelian randomization (MR) to investigate the causal effect of medication use on cutaneous melanoma risk. Exposure data were based on self-reported medication uses from ~320,000 European participants in the UK Biobank. The outcomes included GWAS results from 2824 cutaneous melanoma cases. Single-nucleotide polymorphisms (SNPs) significantly associated with medication use were used as instruments and analyzed with IVW, weighted median, weighted mode, and MR-Egger methods. Sensitivity analyses were used to assess pleiotropy and heterogeneity. Results: The analysis revealed that genetically predicted high use of adrenergics, inhalers, glucocorticoids, and opioids was suggestively associated with a reduced risk of cutaneous melanoma. Sensitivity analyses supported the robustness of these findings, showing no evidence of horizontal pleiotropy or influence from outliers. Conclusions: The results presented herein suggest that certain medication uses may lower the risk of developing cutaneous melanomas, offering potential new avenues for future prevention and treatment strategies. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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Review

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17 pages, 1514 KB

Open AccessReview

A Holistic Approach to Unravel Keloid Pathogenesis and Optimize Therapeutic Outcomes

by Zhendong Cao and Wei Liu

Biomedicines 2026, 14(4), 809; https://doi.org/10.3390/biomedicines14040809 - 2 Apr 2026

Viewed by 589

Abstract

Although tremendous progress has been made over the past decades in elucidating the mechanisms of keloid formation and developing therapeutic interventions, keloid remains challenging to cure and prone to recurrence. Historically, keloid has been regarded as a benign skin tumor, with mechanistic investigations and therapeutic efforts focused primarily on keloid tissue and cells themselves. In contrast, Traditional Chinese Medicine (TCM) posits that skin diseases manifest from internal bodily dysfunction or dysregulation. Inspired by the holistic principles of TCM, together with the literature reports and clinical evidence of keloid constitution (a systemic condition characterized by an individual’s predisposition to keloid formation), we propose that keloid is likely a pseudo-skin tumor profoundly influenced by its pathological microenvironment. Accordingly, we propose keloid as a persistent inflammation-driven proliferative skin disorder, and elimination of the inflammatory microenvironment may be essential for curing keloid and preventing relapse. Based on this concept, we developed a holistic therapeutic approach that combines systemic treatment targeting keloid constitution with local therapies, including surgery, chemo/radiotherapy, and compression therapy, for the keloid lesion itself. The systemic component encompasses lifestyle and dietary modifications, stress management, physical exercise, as well as the oral administration of TCM herbal medicines and small chemical compounds to suppress systemic inflammatory and fibrotic status, thereby improving keloid constitution. This article introduces this novel holistic approach along with supportive case studies. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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33 pages, 1887 KB

Open AccessReview

Dissecting Cellulitis of the Scalp: Linking Pathogenesis to Therapy

by Mislav Mokos, Mirna Šitum and Ines Sjerobabski Masnec

Biomedicines 2026, 14(3), 570; https://doi.org/10.3390/biomedicines14030570 - 2 Mar 2026

Viewed by 1882

Abstract

Dissecting cellulitis of the scalp (DCS) is a chronic, inflammatory follicular occlusion disorder characterized by painful nodules, abscesses, and sinus tracts that lead to scarring alopecia. The therapeutic goal is to limit disease progression and the extent of scarring. Although DCS is traditionally managed with systemic retinoids, antibiotics, and surgical interventions, therapeutic responses are variable and long-term remission remains challenging. Recent insights into the immunological overlap between DCS, hidradenitis suppurativa (HS), and other autoinflammatory follicular disorders have expanded therapeutic options, particularly with biologic agents targeting tumor necrosis factor alpha (TNF-α), interleukin (IL)-17, and IL-23 pathways, as well as Janus kinase (JAK) inhibitors. This review synthesizes the current evidence on medical, procedural, and emerging targeted therapies for DCS, incorporating data from case reports, case series, retrospective cohorts, and recent systematic reviews up to 2025. Special emphasis is placed on the evolving role of biologics and small-molecule inhibitors, which show growing promise for refractory or syndromic presentations. Current evidence supports a stepwise, phenotype-driven approach in which systemic retinoids remain first-line systemic therapy, while biologics represent a rational and increasingly evidence-supported option for moderate-to-severe, treatment-resistant, or syndromic disease. Further controlled studies are needed to define optimal sequencing, duration, and combination strategies for long-term management. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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22 pages, 1024 KB

Open AccessReview

Epigenetic Regulation of Sebaceous and Meibomian Glands: From Development to Disease

by Xuming Zhu and Sixia Huang

Biomedicines 2026, 14(2), 468; https://doi.org/10.3390/biomedicines14020468 - 20 Feb 2026

Cited by 1 | Viewed by 1172

Abstract

Sebaceous glands (SGs) and their specialized subtype, Meibomian glands (MGs), play essential roles in skin and ocular surface homeostasis by producing lipids that maintain barrier integrity and stabilize the tear film. Dysregulation of SG and MG biology contributes to a spectrum of disorders, ranging from benign hyperplasia to sebaceous carcinoma and age-related MG dysfunction. Accumulating evidence highlights the importance of epigenetic regulation, including histone modifications, DNA methylation, and non-coding RNAs (ncRNAs), in controlling SG and MG development, homeostasis, and disease susceptibility. Notably, histone modifiers and ncRNAs modulate acinar differentiation, lipid synthesis, and progenitor cell function. Despite these advances, many epigenetic mechanisms, such as histone lactylation, sumoylation, and phosphorylation, remain underexplored, and several common SG/MG disorders, including chalazion and seborrhea, lack mechanistic studies at the epigenetic level. This review synthesizes current knowledge on SG and MG biology, emphasizing epigenetic regulation, and highlights critical gaps to guide future research aimed at improving the understanding and treatment of SG- and MG-related disorders. Full article

(This article belongs to the Special Issue Pathophysiology and Therapeutic Innovations in Skin and Appendage Disorders)

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