Skin aging, gene expression and calcium

Rinnerthaler, Mark; Streubel, Maria Karolin; Bischof, Johannes; Richter, Klaus

doi:10.1016/j.exger.2014.09.015

Cited by 67 publications

(54 citation statements)

References 95 publications

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“…В то вре-мя как ультрафиолетовое излучение может вызвать акантолизис в эпидермисе у больных с БГХХ, иссле-дователи добились успеха с помощью фототерапии. Однако основным недостатком такого лечения яв-ляются сложности полного облучения в связи с труднодоступностью очагов поражения [6].…”

Section: лечениеunclassified

“…Модифициро-ванный метод прямой иммунофлюоресценции, ста-билизирующий иммунные комплексы, позволил в биоптатах кожи больных с БГХХ выявить раствори-мые иммунные комплексы, содержащие иммуно-глобулин класса G, по десмосомам многослойного плоского эпителия [5]. В настоящее время всесто-ронне изучается роль снижения эпидермального кальция [6,7]. Указанные патогенетические факто-ры в определенной степени позволяют объяснить возможность развития БГХХ без наследственной предрасположенности [8][9][10][11].…”

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Benign chronic Hailey—Hailey pemphigus without proven genetic predisposition

Хамаганова¹,

Померанцев²,

Новожилова³

et al. 2015

Klin. dermatol. venerol.

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Section: лечениеunclassified

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Benign chronic Hailey—Hailey pemphigus without proven genetic predisposition

Хамаганова¹,

Померанцев²,

Новожилова³

et al. 2015

Klin. dermatol. venerol.

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“…For this reason, mutations in keratin genes (KRT) lead to various threatening skin diseases, such as epidermolysis bullosa simplex, which is due to mutations in either KRT5 or KRT14 [3]. Epidermal keratinocytes progress from the basal to the cornified layers, allowing for the regeneration of epidermis within 60 days in an average adult [4]. Accordingly, keratinocyte gene expression undergoes robust longitudinal changes, which is particularly well understood and characterized for keratins [2,[5][6][7].…”

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confidence: 99%

“…The terminal differentiation of the waterrepellent and antibiotic stratum corneum happens in the stratum granulosum and stratum corneum [8]. It involves the release of lamellar bodies leading to an extracellular, highly-ordered lipid matrix that consists of ceramides, cholesterol, and fatty acids [9] and the intracellular aggregation of an envelope composed of keratins, involucrin, filaggrin, and loricrin [4,8]. The lipid matrix serves as a bedding for corneocytes and the proteinaceous envelope in corneocytes adds mechanical stability.…”

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confidence: 99%

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In vitro skin three-dimensional models and their applications

Klicks

Molitor

Ertongur-Fauth

et al. 2017

JCB

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Abstract. Skin fulfils a plethora of eminent physiological functions ranging from physical barrier over immunity shield to the interface mediating social interaction. Prone to several acquired and inherited diseases, skin is therefore a major target of pharmaceutical and cosmetic research. The lack of similarity between human and animal skin and rising ethical concerns in the use of animal models have driven the search for novel realistic three-dimensional skin models. This review provides a survey of contemporary skin models and compares them in terms of applicability, reliability, cost and complexity.Keywords: Skin, phenotypic screening, 3D models, pharmaceutical research Skin -composition and functionHuman skin covers an area of almost 2 m 2 in the adult and consists of the three major layers, subcutis, dermis, and epidermis. The subcutis is composed of adipose and epithelial cells. It harbours blood vessels, neurites of peripheral neurons, Vater-Pacini mechanosensors, and, partially, also sweat glands and hair follicles. It connects the skin to periosteum and fascia, absorbs forces, and mediates thermal insulation. The dermis supplies the epidermis with mechanical support and nutrients. It is stratified into an inner, reticular, and an outer, papillary, zone. The dermis houses most sebaceous glands, sweat glands, hair follicles, smooth muscle cells, and capillary beds and, thus, regulates skin moisture, body temperature, and performs the secretory function of skin. The papillary layer is characterized by relatively loose connective tissue, where Meissner corpuscles sense touch. Immune cells, particularly mast cells and dendritic cells, are patrolling in the papillary layer and mediate local inflammatory reactions and immune surveillance. Finally, dermal fibroblasts secrete extracellular matrix (ECM) and basement membrane components. These are primarily collagens I and III, and a proteoglycan-rich ground substance [1]. The resulting ECM mediates tensile strength of the dermis. The dermo-epidermal junction is centered around a special basement membrane. This is composed of a laminin/collagen IV scaffold and further typical basement membrane components such as perlecans and nidogens [1].The epidermis is a squamous epithelium of 50-100 m thickness. It is devoid of blood vessels but contains keratinocytes, Merkel cell mechanosensors, Langerhans immune cells, and melanocytes. The 1 These authors contributed equally.

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Eczematous Drug Eruptions: Identification and Management of Pharmacological Culprits in Primary Care

Gofman,

Tocci,

Fischer

et al. 2024

Dermatological Reviews

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IntroductionEczematous drug eruptions (EDEs) can mimic common skin conditions like eczema or psoriasis, complicating diagnosis and treatment. These eruptions often present as papular or vesicular lesions, sometimes pruritic, with scaling and crusting. EDEs can manifest anywhere from days to years after initiating medications commonly prescribed in the primary care setting such as calcium channel blockers, ACE inhibitors, ARBs, thiazides, and statins. Misdiagnosis can lead to prolonged patient discomfort and unnecessary treatments. This review emphasizes the importance of accurate differentiation between EDEs and other dermatoses for improved patient outcomes.ObjectiveThis review aims to aid clinicians in the differentiation of EDEs from clinically similar conditions, such as eczema and psoriasis. It focuses on identifying commonly prescribed medications in primary care settings that trigger EDEs, discusses diagnostic strategies, and explores effective treatment options for managing these eruptions.MethodsA comprehensive literature review was conducted using databases such as PubMed, Google Scholar, and the Cochrane Library, covering the period from January 1980 to January 2023. The search included terms like “eczematous,” “drug eruption,” “medication,” “drug induced,” “skin reactions,” “adverse cutaneous,” and “side effects.” Studies selected for review included literary reviews, systematic reviews, case reports, and case series focusing on the pharmacological agents responsible for EDEs. Articles were selected based on their focus on primary care medications and their connection to EDEs.ResultsThe review identified a broad spectrum of medications implicated in EDEs, including calcium channel blockers, ACE inhibitors, ARBs, thiazides, and statins. Among these, calcium channel blockers were the most frequently associated with chronic, diffuse, and pruritic scaly papules and plaques. Other common offenders include ACE inhibitors and ARBs, which primarily trigger eczema‐like rashes in elderly patients. Thiazide diuretics were associated with photosensitivity reactions leading to eczematous eruptions. Statins were found to compromise the skin barrier, contributing to the development of eczematous reactions, particularly in older individuals. The histopathological findings across cases frequently showed spongiosis, eosinophilic infiltrates, and acanthosis, complicating the differentiation from eczema without a thorough medication history.ConclusionsEarly recognition and differentiation of EDEs from common dermatoses, such as eczema or psoriasis, are essential for effective treatment. The review underscores the importance of maintaining a high index of suspicion for drug‐induced eruptions in patients on common cardiovascular medications. Prompt discontinuation of the offending drug, combined with alternative treatments, can significantly improve patient outcomes. Dermatologists and primary care providers should collaborate to optimize treatment, particularly when polypharmacy is a factor. Further research is needed to improve the understanding of the mechanisms behind EDEs and to refine diagnostic strategies, thus minimizing patient morbidity.

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Skin aging, gene expression and calcium

Cited by 67 publications

References 95 publications

Benign chronic Hailey—Hailey pemphigus without proven genetic predisposition

Benign chronic Hailey—Hailey pemphigus without proven genetic predisposition

In vitro skin three-dimensional models and their applications

Eczematous Drug Eruptions: Identification and Management of Pharmacological Culprits in Primary Care

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