摘要
器官纤维化是细胞外基质病理性沉积导致器官功能衰退的终末病理过程。钙黏蛋白-11(cadherin-11,CDH-11)作为经典钙依赖性细胞间黏附分子,在多器官纤维化进程中发挥核心调控作用。在肺、肝、心、肾及皮肤纤维化的小鼠模型中,CDH-11表达水平呈现一致性升高;通过特异性靶向CDH-11可干预多种纤维化小鼠模型,并证实其是跨组织纤维化进程的共同介质。尽管CDH-11靶向治疗在临床前研究中表现突出,但需进一步探索其在人体中的疗效及安全性。
Organ fibrosis is the terminal pathological process characterized by pathological extracellular matrix deposition leading to progressive organ dysfunction.Cadherin-11(CDH-11),a classical calcium-dependent cell adhesion molecule,plays a central regulatory role in the progression of fibrosis across multiple organs.In murine models of fibrosis affecting the lungs,liver,heart,kidneys,and skin,CDH-11 expression is consistently upregulated.Targeting CDH-11 specifically has been shown to mitigate fibrosis in various mouse models,confirming it as a shared mediator in inter-organ fibrotic processes.Although CDH-11-targeted therapies have shown promising outcomes in preclinical studies,further investigation is needed to evaluate their efficacy and safety in humans.
作者
何柔
吴红赤
HE Rou;WU Hongchi(Department of Nephrology,First Affiliated Hospital of Harbin Medical University,Harbin 150001,China)
出处
《临床与病理杂志》
2025年第2期222-229,共8页
Journal of Clinical and Pathological Research
