心血管疾病（CVD）是全球死亡和致残的首要疾病，其机制和治疗研究依赖于有效的疾病模型，但传统2D细胞培养和动物模型因种属差异和病理机制的不同，一定程度上限制其临床转化。近年来，诱导多能干细胞（iPSC）与类器官技术的融合为心血管研究开辟新范式，通过体细胞重编程获得患者特异性iPSC，结合3D生物打印与微流控技术，成功构建出具备电传导、收缩功能和血管网络的心脏类器官及多器官芯片系统。这些模型不仅能精准模拟心肌损伤、动脉粥样硬化等疾病的动态进程，还可用于药物心脏毒性的评估、构建疾病模型，以及疾病机制的探索和再生医学等。然而，当前技术仍存在类器官成熟度低、批次间异质性和神经-免疫微环境缺失等瓶颈。未来研究将聚焦于生物工程的建立、多疾病微环境构建，以及CRISPR-Cas9基因编辑联合移植治疗等方面，以推动心血管精准医疗与再生医学的临床转化。

Cardiovascular disease (CVD) remains the leading cause of global mortality and disability, and its mechanisms and treatment research rely on effective disease models. However, the clinical translation of research findings has been limited by the inherent constraints of traditional two-dimensional cell cultures and animal models, which often fail to fully recapitulate human pathophysiology due to interspecies differences. In recent years, the convergence of induced pluripotent stem cell (iPSC) technology and organoid systems has established a transformative paradigm for cardiovascular research. By reprogramming patient-derived somatic cells into iPSC and leveraging three-dimentional bioprinting and microfluidic platforms, researchers have successfully engineered cardiac organoids and multi-organ chip systems that exhibit functional electrophysiology, contractility, and vascular networks. These advanced models not only faithfully replicate dynamic disease processes, such as myocardial injury and atherosclerosis, but also enable applications in drug cardiotoxicity assessment, disease modeling, mechanistic investigations and regenerative medicine. Nevertheless, critical challenges persist, including low organoid maturity, batch-to-batch heterogeneity, and the absence of neuro-immune crosstalk in current systems. Future research will focus on bioengineering innovations, constructing multi-disease microenvironments, and combinatorial approaches like CRISPR-Cas9 gene editing coupled with transplantation therapy to accelerate the translation of precision medicine and regenerative therapies for CVD.