Abstract：
BACKGROUND: Psoriasis is a chronic disease of inflammatory nature. It involves autoimmune mechanism and the systemic diseased state is created by the interaction of immune system, autoantigens and variety of environmental triggers. It is a complex skin disease which involves participation of numerous factors, making it multifactorial in nature. The main characteristics include proliferation of keratinocytes, increase in dermal vascularity and infiltrated immune cells. Among all factors, vascular alterations present a significant feature of the disease and angiogenesis seems to have an important role in giving rise to psoriasis phenotype. In the early phases of psoriasis there occurs sprouting of new blood vessels which disappear with disease clearance. Psoriatic lesions show highly altered vascular network in the form of numerous enlarged, tortuous and hyperpermeable cutaneous blood vessels. Secretion of various pro-angiogenic growth factors promote the expansion of vascular network in psoriatic skin cells. In addition to pro-angiogenic growth factors, pro-inflammatory cytokines also contribute to this process by activating endothelial cells and exerting pro-angiogenic action as well. Angiogenesis, in psoriasis display a close association of vascular endothelium activation, angiogenesis, inflammation and lesional skin, as is demonstrated by in vivo models.
OBJECTIVE: The present review discusses angiogenesis as the central process in the evolution of psoriasis and summarizes various angiogenic mediators and their respective roles in the development of psoriasis.
CONCLUSIONS: Anti-angiogenic therapies targeting vasoproliferation may represent a valid approach for the development of anti-psoriatic drugs and further development in this field can pave way to new fields of treatment. Such therapies could be at par to those directly targeting inflammation.
OBJECTIVE: The present review discusses angiogenesis as the central process in the evolution of psoriasis and summarizes various angiogenic mediators and their respective roles in the development of psoriasis.
CONCLUSIONS: Anti-angiogenic therapies targeting vasoproliferation may represent a valid approach for the development of anti-psoriatic drugs and further development in this field can pave way to new fields of treatment. Such therapies could be at par to those directly targeting inflammation.
摘要：
背景：银屑病是一种慢性炎症性疾病。它涉及自身免疫机制，全身性疾病状态是由免疫系统的相互作用产生的，自身抗原和各种环境触发因素。这是一种复杂的皮肤病，涉及多种因素的参与，使其本质上是多因素的。主要特征包括角质形成细胞的增殖，增加真皮血管和浸润的免疫细胞。在所有因素中，血管改变是该疾病的重要特征，血管生成似乎在引起牛皮癣表型中具有重要作用。在牛皮癣的早期阶段，发生新血管的发芽，随着疾病的清除而消失。银屑病病变表现出高度改变的血管网络，以大量扩大的形式，曲折和高渗透的皮肤血管。各种促血管生成生长因子的分泌促进银屑病皮肤细胞中血管网络的扩张。除了促血管生成生长因子，促炎细胞因子也通过激活内皮细胞和发挥促血管生成作用而有助于该过程。血管生成,在牛皮癣中显示出血管内皮活化的密切关系，血管生成,炎症和皮损,正如体内模型所证明的那样。
目的：本文讨论了血管生成是银屑病发展的核心过程，并总结了各种血管生成介质及其在银屑病发展中的作用。
结论：以血管增殖为目标的抗血管生成疗法可能是开发抗银屑病药物的有效方法，该领域的进一步发展可以为新的治疗领域铺平道路。这种疗法可以与直接靶向炎症的疗法相当。
目的：本文讨论了血管生成是银屑病发展的核心过程，并总结了各种血管生成介质及其在银屑病发展中的作用。
结论：以血管增殖为目标的抗血管生成疗法可能是开发抗银屑病药物的有效方法，该领域的进一步发展可以为新的治疗领域铺平道路。这种疗法可以与直接靶向炎症的疗法相当。
