Jeffrey Rajkumara Neha Chandana Peter Liob Vivian Shic
a Department of Dermatology, University of Illinois at Chicago College of Medicine, Chicago, IL, USA;
b Department of Dermatology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA;
c Department of Dermatology, University of Arkansas for Medical Sciences, Little Rock, AK, USA
Keywords
Skin barrier · Barrier disruption · Moisturizers
Abstract
Background: The anatomic layers of the skin are well-defined, and a functional model of the skin barrier has recently been described. Barrier disruption plays a key role in several skin conditions, and moisturization is recommended as an initial treatment in conditions such as atopic dermatitis. This review aimed to analyze the skin barrier in the context of the function model, with a focus on the mechanisms by which moisturizers support each of the functional layers of the skin barrier to promote homeostasis and repair. Summary: The skin barrier is comprised of four interdependent layers – physical, chemical, microbiologic, and immunologic – which maintain barrier structure and function. Moisturizers target disruption affecting each of these four layers through several mechanisms and were shown to improve transepidermal water loss in several studies. Occlusives, humectants, and emollients occlude the surface of the stratum corneum (SC), draw water from the dermis into the epidermis, and assimilate into the SC, re- spectively, in order to strengthen the physical skin barrier. Acidic moisturizers bolster the chemical skin barrier by sup-porting optimal enzymatic function, increasing ceramide production, and facilitating ideal conditions for commensal microorganisms. Regular moisturization may strengthen the immunologic skin barrier by reducing permeability and subsequent allergen penetration and sensitization. Key Messages: The physical, chemical, microbiologic, and im-munologic layers of the skin barrier are each uniquely impacted in states of skin barrier disruption. Moisturizers target each of the layers of the skin barrier to maintain homeostasis and facilitate repair.
Mauro Gitto1,2 · Federica Catapano1,2 · Marco Francone1,2 · Gianluca Mincione1,2 · Vincenzo Scialò1,2 ·Carlo A. Pivato1,2 · Costanza Lisi1,2 · Damiano Regazzoli1,2 · Davide Cao1,2 · Roberta Maria Fiorina1 ·Alessandra Petrelli3,4 · Loredana Bucciarelli4 · Cristian Loretelli3,4 · Gianluigi Condorelli1,2 · Paolo Fiorina3,4,5 · Giulio Stefanini1,2
Received: 4 October 2025 / Accepted: 15 October 2025 / Published online: 4 November 2025 © The Author(s) 2025
Background Despite advances in therapeutic strategies a significant proportion of acute coronary syndrome (ACS) patients experience early coronary artery disease (CAD) progression, particularly those with diabetes.
Aim To evaluate CAD progression in diabetic patients treated with glucagon-like peptide 1 receptor agonists (GLP-1Ra) over 1 year after an ACS.
Methods Patients presenting with non–ST-elevation ACS between 2019 and 2022 were enrolled in a prospective registry and underwent serial coronary computed tomography angiography (CCTA) at baseline (after revascularization, during the index hospitalization) and at 1-year follow-up. The primary endpoint was the absolute change (1 year – baseline) in non-culprit lesion plaque burden (ΔPB) on CCTA, with the absolute change in patient percent atheroma volume (ΔPAV) as a key secondary endpoint. A comprehensive lipidomic, metabolomic, and proteomic plasma assessment was also performed in all GLP-1Ra–treated patients and four randomly selected controls.
Results Of 28 diabetic patients, 7 (25%) with 22 coronary plaques were treated with GLP-1Ra, and 21 (75%) with 65 plaques received other antidiabetic agents. In the 1-year observation frame, both ΔPB (-5.8±12.8% vs. -1.1±13.6%, p=0.041) and ΔPAV (-6.1% [-7.3, -1.8] vs. -0.7% [-2.4, 9.8], p=0.039) were significantly lower in GLP-1Ra-treated patients. Total atheroma volume also showed a numerically greater reduction in the GLP-1Ra cohort (0.7 mm³ [-2.5-8.7] vs. 25.0 mm³ [4.8–39.7]), primarily due to a decrease in plaque fibrofatty volume percentage (-2.9±10.1% vs. 1.0±6.8%, p=0.042). Lipi-domic, metabolomic, and proteomic analyses identified reductions in monoacylglycerols and triacylglycerols, increases in diacylglycerols and phosphatidylethanolamine, a shift from carbohydrate metabolism toward lipid metabolism and hormone regulation, and differential expression of proteins involved in complement activation, endothelial function, and cytoskeletal organization in GLP-1Ra–treated patients compared with controls.
Conclusions In diabetic patients with ACS, GLP-1Ra therapy was associated with a significant regression in coronary plaque burden at 1 year, supported by favorable lipidomic, metabolomic, and proteomic changes. These findings suggest a potential role for GLP-1Ra in modifying atherosclerosis progression beyond glycemic control.
Keywords GLP-1 receptor agonists · Diabetes mellitus · Coronary artery disease · Acute coronary syndrome · Plaque regression
This article is excerpted from the 《Frontiers in Psychology》 by Wound World
伤口世界平台生态圈,以“关爱人间所有伤口患者”为愿景,连接、整合和拓展线上和线下的管理慢性伤口的资源,倡导远程、就近和居家管理慢性伤口,解决伤口专家的碎片化时间的价值创造、诊疗经验的裂变复制、和患者的就近、居家和低成本管理慢性伤口的问题。
2019广东省医疗行业协会伤口管理分会年会
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