Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

Abstract

Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

SIRT3 deficiency delays diabetic skin wound healing via oxidative stress and necroptosis enhancement

“…Previous studies have verified that moderate oxidative stress is essential for skin wound healing . On the contrary, excessive oxidative stress delays skin wound healing especially in DM by inhibiting angiogenesis, regulating extracellular matrix deposition and disordering cytokine activity .…”

The diabetic dental pulp repair: involvement of vascular endothelial growth factor and bone morphogenetic protein 2

“…Hydroxyl ions exhibit antibacterial properties due to alcaline reaction and stimulates reparative dentin formation [19]. Oxidation of hydroxyl ions results in formation of hydroxyl radicals, which is able, as reactive oxygen species (ROS), to induce VEGF expression [20]. Beside ROS, another potent stimulus for VEGF induction is hypoxia.…”

The role of homocysteine and other endogenous intoxication markers in the pathogenesis of lichen planus

“…To assess the intensity of protein peroxidation, the level of carbonyl groups should be determined 16 . Free radical oxidation of proteins results in oxidative DNA damage and modifications of gene transcription leading to mutations, synthesis of abnormal surface molecules, increased protein immunogenicity, and increased probability of autoantibody synthesis 17,20 . MMWPs are medium molecules, endogenous components with molecular weight 500-5000 Da.…”

“…Since the range of factors leading to endogenous intoxication in LP has not been fully determined yet, the indices of metabolic products and their role in the development of endo-toxicosis processes should be investigated 20 . Hence, publications on homocysteine and its role as endogenous toxin in the pathogenesis of chronic skin diseases warrant attention 21,22 .…”