Endothelial Piezo1 mediates barrier dysfunction and NLRP3 inflammasomes activation in psoriasis.

Psoriasis is a chronic inflammatory skin disease characterized by abnormal dilation of microvessels in the dermal papillary layer. Multiple studies have demonstrated that vascular endothelial cells regulate vascular function rather than merely acting as passive barriers. Piezo1 serves as a critical mechanical switch, sensing mechanical changes induced by vasodilation.

Targeting the Galectin-7/TRPM2/Zn/DRP-1 Signaling Pathway: A Potential Therapeutic Intervention in the Pathogenesis of SJS/TEN.

Background: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) represent a spectrum of severe drug-induced cutaneous reactions. These conditions are characterized by widespread and confluent keratinocyte apoptosis, which differentiates them from erythema multiforme (EM). Mounting evidence has implicated the mitochondrial-dependent apoptosis pathway in the pathogenesis of SJS/TEN, but the potential roles and specific mechanisms of these pathways in SJS/TEN remain largely unexplored.

Exosomal mediated lipid metabolism, ferritinophagy and CoQ-dependent pathway contributes to the ferroptosis of keratinocyte in SJS/TEN.

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) manifest life-threatening cutaneous adverse drug reactions characterized by keratinocyte death. Previous studies have indicated that apoptosis and necroptosis are implicated in SJS/TEN pathogeneses. However, other forms of cell death involved in this process remain unidentified.

NLRX1 deficiency exacerbates skin inflammation in atopic dermatitis by disrupting mitophagy.

NLRX1 is an important regulator of inflammatory signaling in innate immune cells. Recent studies indicate NLRX1 activation may be a novel mechanism for inflammatory diseases, however, it has not been explored in atopic dermatitis (AD). Our study aims to investigate the potential role of NLRX1 in the pathogenesis of AD.

Eosinophil extracellular traps drive T follicular helper cell differentiation via VIRMA-dependent MAF stabilization in bullous pemphigoid.

Background: Bullous pemphigoid (BP) is an autoimmune blistering disease characterized by the presence of pathogenic autoantibodies and a substantial influx of immune cells into skin lesions. However, the role of eosinophils in BP remains inadequately elucidated.

Objective: We sought to determine the pathologic involvement of eosinophils and eosinophil extracellular traps (EETs) in BP.

Endothelial Dysfunction in Psoriasis: An Integrative Review.

Vascular endothelial cells (ECs), the inner layer of blood vessels, were previously considered to be a passive lining that facilitates cellular and molecular exchange. However, recent studies have revealed that ECs can respond to various stimuli and actively regulate vascular function and skin inflammation. Specific subtypes of ECs are known to have significant roles in a diverse range of physiological and pathological processes in the skin.

Keratin 17 covalently binds to alpha-enolase and exacerbates proliferation of keratinocytes in psoriasis.

Dysregulated glucose metabolism is an important characteristic of psoriasis. Cytoskeletal protein keratin 17 (K17) is highly expressed in the psoriatic epidermis and contributes to psoriasis pathogenesis. However, whether K17 is involved in the dysregulated glucose metabolism of keratinocytes (KCs) in psoriasis remains unclear.

CXCL12/CXCR4 Axis Drives the Chemotaxis and Differentiation of B Cells in Bullous Pemphigoid.

Bullous pemphigoid (BP) is an autoimmune bullous skin disease characterized by autoantibodies against the hemidesmosomal proteins in the skin and mucous membranes. The efficiency of B-cell‒targeting biologics in BP indicates the important role of B cells in its pathogenesis. However, abnormal B-cell migration and differentiation in BP require further elucidation.

LCN2 Mediates Skin Inflammation in Psoriasis through the SREBP2‒NLRC4 Axis.

Lipocalins are a family of secreted adipokines that regulate cell lipid metabolism and immune responses. Although we have previously revealed that LCN2 modulates neutrophil activation in psoriasis, the other roles of LCN2 in psoriatic local inflammation have remained elusive. In this study, we found that 24p3R, the well-known specific receptor of LCN2, was highly expressed in the lesional epidermis of patients with psoriasis.

Keratin 17 Is Required for Lipid Metabolism in Keratinocytes and Benefits Epidermal Permeability Barrier Homeostasis.

The epidermal barrier refers to the stratum corneum, the uppermost layer of the skin, and constitutes the first line of defense against invasion by potentially harmful pathogens, diminishes -epidermal water loss, and plays a crucial role in the maintenance of skin homeostasis. Keratin 17 (K17) is a type I epithelial keratin with multiple functions, including in skin inflammation, epithelial cell growth, protein synthesis, and tumorigenesis. However, the relationship between K17 and the skin barrier has yet to be systematically investigated.

Enhanced phenotype of calcipotriol-induced atopic dermatitis in filaggrin-deficient mice.

Impaired function of filaggrin (FLG) is a major predisposing factor for atopic dermatitis (AD). Several studies on FLG-deficient (Flg ) mice have indicated an essential role for FLG in the skin barrier and the development of AD, but none of the studies have described the characteristics on Flg mice with calcipotriol (CPT)-induced atopic dermatitis, which restricts the comprehensive understanding of functions of FLG. The present study sought to generate Flg mice and applied CPT to produce AD-like dermatitis for in vivo analysis of the FLG functions.