白癜风(vitiligo)多因表皮中黑素细胞丢失或功能低下而形成色素脱失斑,其具体机制尚未完全阐明.近来黑素细胞自噬学说以及黑素细胞脱落(melanocytorrhagy)学说趋于成熟.黑素细胞自噬学说支持者认为自噬水平低下可能破坏黑素细胞抗氧化防御系统从而导致白癜风发病;黑素细胞脱落学说指出,非节段型白癜风(non-segmental vitiligo,NSV)患者表皮内由于上皮型钙黏素(E-cadherin,Ecad)所介导的细胞间黏附异常可引起黑素细胞与邻近角质形成细胞之间出现黏附缺陷,加之机械应力等作用后通过影响多种胞内信号,黑素细胞自基底层逃逸,最终经表皮丢失.本文将黑素细胞自噬与黑素细胞脱落的研究进展,以及两者间可能存在的相关性作一概述,为非节段型白癜风发病机制和靶向治疗提供方向.“,”Vitiligo due to the loss of melanocytes in the epidermis or dysfunction of the formation of clinical common pigmentation spots, the specific mechanism has not yet fully elucidated. Recent studies of melanocytic autophagy and melanocytorrhagy have matured.Low level of autophagy may damage the melanocyte antioxidant defense system leading to vitiligo. Researchers who support for melanocyte shedding theory pointed out that non-segmental vitiligo(NSV) Epithelial cadmium(Ecad) within the epidermis mediated intercellular adhesion abnormalities, which can cause melanocytes and adjacent keratinocytes between Adhesion defects, then combined with mechanical stress and other effects through the impact of a variety of intracellular signals, melanocytes from the base layer to escape, and ultimately lost through the epidermis. This article will make an overview about the research progress of melanocyte autophagy and melanocyte shedding, and the possible correlation between the two theories.They may provide a direction for the pathogenesis of non-segmental vitiligo and targeted therapy.