Kang Sewon, Cho Soyun, Chung Jin Ho, Hammerberg Craig, Fisher Gary J, Voorhees John J
Department of Dermatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Am J Pathol. 2005 Jun;166(6):1691-9. doi: 10.1016/s0002-9440(10)62479-0.
Acne is the most common skin disease, causing significant psychosocial problems for those afflicted. Currently available agents for acne treatment, such as oral antibiotics and isotretinoin (Accutane), have limited use. Thus, development of novel agents to treat this disease is needed. However, the pathophysiology of acne inflammation is poorly understood. Before new therapeutic strategies can be devised, knowledge regarding molecular mechanisms of acne inflammation is required. We report here that transcription factors nuclear factor-kappaB and activator protein-1 are activated in acne lesions with consequent elevated expression of their target gene products, inflammatory cytokines and matrix-degrading metalloproteinases, respectively. These elevated gene products are molecular mediators of inflammation and collagen degradation in acne lesions in vivo. This new knowledge enables a rational strategy for development of pharmacological agents that can target the inflammation and matrix remodeling that occurs in severe acne.
痤疮是最常见的皮肤病，给患者带来严重的心理社会问题。目前用于治疗痤疮的药物，如口服抗生素和异维甲酸（泰尔丝），用途有限。因此，需要开发治疗这种疾病的新型药物。然而，痤疮炎症的病理生理学尚不清楚。在设计新的治疗策略之前，需要了解痤疮炎症的分子机制。我们在此报告，转录因子核因子-κB和活化蛋白-1在痤疮皮损中被激活，其靶基因产物、炎性细胞因子和基质降解金属蛋白酶的表达随之升高。这些升高的基因产物是体内痤疮皮损中炎症和胶原蛋白降解的分子介质。这一新知识为开发能够靶向重度痤疮中发生的炎症和基质重塑的药物提供了合理的策略。
