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Rosacea is a common chronic inflammatory condition primarily affecting middle-aged women. It presents with flushing, erythema, telangiectasia, papules, pustules, phymatous changes, and ocular involvement. Although typically grouped into four subtypes—erythematotelangiectatic, papulopustular, ocular, and phymatous—overlapping features often favor a phenotypic diagnostic approach. Neurogenic rosacea (NR) has emerged as a distinct subgroup featuring distinguishing features such as peripheral facial erythema, severe burning and stinging sensations, and resistance to standard rosacea therapies. Recent insights into the pathophysiology of NR propose neural dysregulation as the main driver of the condition. Specifically, the activation of TRP channels at cutaneous sensory nerve endings in the dermis triggers the release of vasoactive peptides, driving neuroinflammation and resulting in burning and stinging. Additionally, there is a marked association with neuropsychiatric comorbidities, which would further mediate the pathogenesis of the condition. In line with this pathophysiological model, NR often fails to respond to conventional rosacea treatments. Instead, patients benefit more from antidepressants and neuroleptic agents that help modulate neuronal activity and alleviate symptoms. This review explores and summarizes the scientific evidence regarding the new insights on disease pathogenesis, clinical manifestations, and proposed treatments for NR.

Rosacea is a common, chronic facial skin disease; features include erythema, papules, pustules, telangiectasias, flushing, phymatous changes, and ocular manifestations. Management includes avoidance of triggers, skin care measures, and treatments that target various features.

Background The management of papulopustular rosacea presents a significant clinical challenge. Anti‐inflammatory and vasoconstrictive treatments are ineffective in the rapid amelioration of the dryness, burning, and itching caused by skin barrier damage in patients with papulopustular rosacea. Aims To assess the efficacy and safety of the topical application of compound heparin sodium allantoin gel to treat rosacea. Methods Eighty‐two patients participated in this randomized, prospective, single‐center, and controlled trial. The Clinician Erythema Assessment score, Investigator Global Assessment score, transepidermal water loss, and skin hydration were evaluated at 0, 2, 4, 8, and 12 weeks. Rosacea‐specific quality of life score, itching, dryness, burning, Global Aesthetic Improvement Scale, and Patient Self‐Assessment grades were also assessed. Results Compared with the traditional therapy group, the 8‐week and 12‐week topical application of compound heparin sodium allantoin gel to treat rosacea significantly decreased Clinician Erythema Assessment/Investigator Global Assessment grades, burning and itching grades, and rosacea‐specific quality of life scores. Compound heparin sodium allantoin gel significantly improved the skin barrier with hydration and significantly decreased trans‐epidermal water loss. For patients with Demodex infestation, externally applied compound heparin sodium allantoin gel was associated with better rosacea treatment outcomes and improved skin barrier function than externally applied hyaluronic acid. This may be attributable to the inhibition of abnormal demodex, improved skin barrier, and repair of minor skin wounds. Conclusions Compound heparin sodium allantoin gel effectively improved facial erythema, alleviated ithching and burning sensations, and improved patients' quality of life. Trail Registration ClinicalTrials.gov identifier: ChiCTR2400087948

Angiogenesis, the growth of new blood vessels from preexisting vessels, is associated with inflammation in various pathological conditions. Well-known angiogenetic factors include vascular endothelial growth factor (VEGF), angiopoietins, platelet-derived growth factor, transforming growth factor-β, and basic fibroblast growth factor. Yes-associated protein 1 (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) have recently been added to an important angiogenic factor. Accumulating evidence indicates associations between angiogenesis and chronic inflammatory skin diseases. Angiogenesis is deeply involved in the pathogenesis of psoriasis. VEGF, angiopoietins, tumor necrosis factor-a, interleukin-8, and interleukin-17 are unregulated in psoriasis and induce angiogenesis. Angiogenesis may be involved in the pathogenesis of atopic dermatitis, and in particular, mast cells are a major source of VEGF expression. Angiogenesis is an essential process in rosacea, which is induced by LL-37 from a signal cascade by microorganisms, VEGF, and MMP-3 from mast cells. In addition, angiogenesis by increased VEGF has been reported in chronic urticaria and hidradenitis suppurativa. The finding that VEGF is expressed in inflammatory skin lesions indicates that inhibition of angiogenesis is a useful strategy for treatment of chronic, inflammatory skin disorders.

Rosacea is a chronic inflammatory dermatosis predominantly affecting the central face, with its pathogenesis not yet fully elucidated. Macrophages, as innate immune cells in the human body, play a crucial role in inflammatory responses. However, the specific mechanistic role of macrophages in rosacea remains incompletely understood. This review aims to comprehensively analyze and discuss the functions of macrophages, their involvement in the pathogenesis of rosacea, and their potential as therapeutic targets. A systematic literature search was conducted using keywords such as \"rosacea\" and \"macrophage\" in databases including PubMed and Web of Science, without restrictions on article type or publication date, to ensure a comprehensive retrieval of relevant studies. Additionally, the references cited in the retrieved articles were manually searched to gather further pertinent knowledge. For the articles obtained from the database searches, we focused solely on those that mentioned the role of macrophages in rosacea and related therapeutic approaches to ensure the accuracy of the content. Ultimately, 121 articles were selected for inclusion in this review, encompassing review articles, original research studies, meta-analyses, and other types of publications. This review summarizes the latest research progress on the role of macrophages in the pathogenesis of rosacea, emphasizing their significant involvement through the regulation of immune responses, angiogenesis, oxidative stress, fibrosis, and other processes. Furthermore, the potential of macrophages as therapeutic targets for rosacea is explored, which warrants further investigation in the future. Despite the advancements made, numerous unresolved questions remain regarding the mechanistic role of macrophages in rosacea. Future research is imperative to delve deeper into the underlying mechanisms, thereby providing novel insights into the pathogenesis and treatment of rosacea.Please confirm that the below Frontiers AI generated Alt-Text is an accurate visual description of your Figure(s). These Figure Alt-text proposals won't replace your figure captions and will not be visible on your article. If you wish to make any changes, kindly provide the exact revised Alt-Text you would like to use, ensuring that the word-count remains at approximately 100 words for best accessibility results. Further information on Alt-Text can be found here.

Rosacea is a common chronic inflammatory skin disease of the central facial skin and is of unknown origin. Currently, two classifications of rosacea exist that are based on either \"preformed\" clinical subtypes (erythematotelangiectatic, papulopustular, phymatous, and ocular) or patient-tailored analysis of the presented rosacea phenotype. Rosacea etiology and pathophysiology are poorly understood. However, recent findings indicate that genetic and environmental components can trigger rosacea initiation and aggravation by dysregulation of the innate and adaptive immune system. Trigger factors also lead to the release of various mediators such as keratinocytes (for example, cathelicidin, vascular endothelial growth factor, and endothelin-1), endothelial cells (nitric oxide), mast cells (cathelicidin and matrix metalloproteinases), macrophages (interferon-gamma, tumor necrosis factor, matrix metalloproteinases, and interleukin-26), and T helper type 1 (T H1) and T H17 cells. Additionally, trigger factors can directly communicate to the cutaneous nervous system and, by neurovascular and neuro-immune active neuropeptides, lead to the manifestation of rosacea lesions. Here, we aim to summarize the recent advances that preceded the new rosacea classification and address a symptom-based approach in the management of patients with rosacea.

Rosacea is a chronic cutaneous inflammatory disease that affects the facial skin. Clinically, rosacea can be categorized into papulopustular, erythematotelangiectatic, ocular, and phymatous rosacea. However, the phenotypic presentations of rosacea are more heterogeneous. Although the pathophysiology of rosacea remains to be elucidated, immunologic alterations and neurovascular dysregulation are thought to have important roles in initiating and strengthening the clinical manifestations of rosacea. In this article, we present the possible molecular mechanisms of rosacea based on recent laboratory and clinical studies. We describe the genetic predisposition for rosacea along with its associated diseases, triggering factors, and suggested management options in detail based on the underlying molecular biology. Understanding the molecular pathomechanisms of rosacea will likely aid toward better comprehending its complex pathogenesis.

Background Rosacea is more common in women and Caucasians, leading to little research on rosacea in Asian men. Additionally, there is limited research on the patients across different age groups. Aims The aim of this study is to analyze and compare the characteristics of male patients of rosacea among different age groups. Methods A retrospective analysis was conducted on 215 male patients with rosacea, investigating their characteristics, clinical symptoms, exacerbating factors, complications, psychological status, and treatment, as well as exploring factors influencing the early onset of male rosacea. Results The patients were divided into three age groups (≤ 30 years, 31–44 years, and ≥ 45 years), with the study revealing an average age of 38.59 ± 13.13 years among the patients. The most common subtype of rosacea in men was erythematotelangiectatic rosacea (ETR), followed by phymatous rosacea (PhR). The main reported features included persistent erythema (87.4%) and telangiectasia (71.2%), predominantly affecting the nose (58.6%) and cheeks (56.3%). Twenty‐six percent of patients reported concurrent skin diseases, with 14.0% reporting systemic diseases. Significant differences were observed among different age groups regarding family history, clinical features, lesion distribution, symptom severity, aggravating factors, presence of systemic diseases, and treatment preferences. Subjective skin typing, Fitzpatrick phototype, and positive family history were identified as factors influencing the age of onset of rosacea in men. Conclusion Male patients with rosacea exhibit distinct clinical characteristics, with a greater prevalence of nasal involvement and nasal lesions among male patients. Clinical features vary among different age groups, with patients aged ≥ 45 experiencing more complex and severe symptoms. Patients aged ≤ 30 may be more influenced by genetic factors and have higher treatment expectations.

This research elucidates rosacea management with novel insights into probiotic use alongside doxycycline, showing dual benefits in symptom relief and inflammation reduction in patients. The study maps probiotic-induced shifts in gut and skin microbiota, underscoring microbial shifts correlating with skin health improvements. Crucially, it deciphers the gut–skin axis modulation by probiotics, proposing a method to curb antibiotic resistance in rosacea therapies. This study furnishes robust evidence for probiotics in rosacea, advancing our grasp of the gut–skin relationship.

Rosacea, an inflammatory skin disorder with complex pathogenesis, remains poorly understood. Through integrative bioinformatics and experimental approaches, we identified 304 differentially expressed genes in erythrotelangiectasia rosacea (ETR), primarily enriched in lipid metabolism pathways. Support vector machine (SVM), linear regression analyses and network analysis revealed ACADVL and ACSL5 as potential therapeutic targets. Immunological profiling demonstrated distinctive immune cell infiltration, with elevated M0 and M1 macrophages in patients with ETR. Immunofluorescence validation confirmed significant ACSL5 upregulation and increased M1 macrophage infiltration in the rosacea mouse model. The co-localization of ACSL5 with M1 macrophage markers suggests a mechanistic link between lipid metabolism and inflammatory responses. These findings provide new insights into ETR pathogenesis and highlight ACSL5 as a promising therapeutic target for inflammatory skin disorders.