首页|经典Wnt信号通路与心血管疾病

经典Wnt信号通路与心血管疾病

扫码查看
心血管疾病是一组累及心脏和血管的疾病,主要包括冠心病、中风等疾病。它是世界上引起死亡的主要原因之一,其发病率逐年上升。高血压是心血管疾病的主要危险因素。Wnt信号通路由一系列控制基本生物学过程的高度保守的级联事件组成。Wnt信号通路包括经典Wnt通路(或Wnt/β-catenin通路)、非经典平面细胞极性通路和非经典钙依赖通路。异常的Wnt信号通路能够引起和促进细胞增殖和分化、心脏畸形,以及各种恶性肿瘤,因此,以Wnt信号通路为靶点的药物设计具有巨大的治疗潜力。经典Wnt/β-catenin通路通过调节细胞增殖、迁移、凋亡、血脑屏障通透性、炎症、氧化应激和免疫反应等参与动脉粥样硬化、脑卒中等心血管疾病的发生发展。本文结合最新研究进展,综述Wnt/β-catenin信号通路在心血管疾病发生发展中的相关机制,希望为心血管疾病的预防和治疗提供新的思路。
Wnt/β-catenin Signaling Cascades in Cardiovascular Diseases
Cardiovascular diseases are a group of disorders of the heart and blood vessels,primarily including coronary heart disease,stroke,and other diseases.It is the world's leading cause of death,and its incidence is increasing yearly.Hypertension is a major risk factor for cardiovascular disease.Wnt signaling comprises a series of highly conservative cascading events controlling fundamental biological processes.Wnt signaling pathways include the canonical Wnt pathway(or Wnt/β-catenin pathway),the non-canonical planar cell-polarity pathway,and the non-canonical calcium-dependent pathways.Abnormal Wnt signaling promotes cell proliferation and differentiation,cardiac malformations,various malignancies,so drugs targeting Wnt signaling play a great therapeutic potential.Wnt/β-catenin pathway is involved in the occurrence and development of cardiovascular diseases such as atherosclerosis and stroke by regulating cell proliferation,migration,apoptosis,blood-brain barrier permeability,inflammation,oxidative stress,and immune response.Based on the latest research progress,this review summarizes the role of Wnt/β-catenin signaling in cardiovascular diseases,in order to provide new ideas for the prevention and treatment of cardiovascular diseases.

Wnt/β-catenin pathwaycardiovascular diseasespathological process

齐燕飞、刘晏平、许文青、闫小雪

展开 >

中国科学院生物物理研究所,生物大分子国家重点实验室,中国科学院生物大分子卓越中心,北京 100101

中国科学院大学生命科学学院,北京 100049

"上海科技大学,生命科学与技术学院,上海高级免疫化学研究所,上海 201210

Wnt/β-catenin信号通路 心血管疾病 病程

2024

生物化学与生物物理进展
中国科学院生物物理研究所,中国生物物理学会

生物化学与生物物理进展

CSTPCD北大核心
影响因子:0.476
ISSN:1000-3282
年,卷(期):2024.51(10)