心血管和肿瘤疾病是全球主要死因。对于这两种疾病，已经确定了一种新的和广泛的风险因素：克隆造血干细胞增生（CH）。CH被定义为在体细胞突变的基础上外围血细胞的克隆扩展，没有明显的造血系统恶性肿瘤。最常受影响的基因是TET2、DNMT3A、ASXL1和JAK2。到70岁时，至少20-50%的人携带CH克隆，增加40%的全因死亡率，具有惊人的临床影响。这主要是由于心血管风险几乎增加了两倍，但也由于恶性转化风险的增加。患有CH的个体不仅有更高的风险，而且在动脉粥样硬化事件（如中风或心肌梗死）、心力衰竭和心源性休克后的结果更差。升高的细胞因子水平、功能失调的巨噬细胞活性和炎性小体的激活表明，慢性炎症和克隆扩展的恶性循环是主要的功能联系。尽管这种情况显然具有很高的影响力，但对其认识、功能理解和尤其是临床意义仍需要进一步研究。本评述提供了CH及其与心血管和血液疾病的关系的当前知识概述。重点是介绍动脉粥样硬化、炎症和CH之间的基本功能机制，确定进一步研究的问题，并考虑潜在的临床意义。©2022。作者。

Cardiovascular and oncological diseases represent the global major causes of death. For both, a novel and far-reaching risk factor has been identified: clonal hematopoiesis (CH). CH is defined as clonal expansion of peripheral blood cells on the basis of somatic mutations, without overt hematological malignancy. The most commonly affected genes are TET2, DNMT3A, ASXL1 and JAK2. By the age of 70, at least 20-50% of all individuals carry a CH clone, conveying a striking clinical impact by increasing all-cause mortality by 40%. This is due predominantly to a nearly two-fold increase of cardiovascular risk, but also to an elevated risk of malignant transformation. Individuals with CH show not only increased risk for, but also worse outcomes after arteriosclerotic events, such as stroke or myocardial infarction, decompensated heart failure and cardiogenic shock. Elevated cytokine levels, dysfunctional macrophage activity and activation of the inflammasome suggest that a vicious cycle of chronic inflammation and clonal expansion represents the major functional link. Despite the apparently high impact of this entity, awareness, functional understanding and especially clinical implications still require further research. This review provides an overview of the current knowledge of CH and its relation to cardiovascular and hematological diseases. It focuses on the basic functional mechanisms in the interplay between atherosclerosis, inflammation and CH, identifies issues for further research and considers potential clinical implications.© 2022. The Author(s).