Clonal hematopoiesis of indeterminate potential (CHIP) is the presence of a clonally expanded hematopoietic stem cell caused by a leukemogenic mutation in individuals without evidence of hematologic malignancy, dysplasia, or cytopenia. CHIP is associated with a 0.5–1.0% risk per year of leukemia. Remarkably, it confers a two-fold increase in cardiovascular risk independent of traditional risk factors. Roughly 80% of patients with CHIP have mutations in epigenetic regulators DNMT3A, TET2, ASXL1, DNA damage repair genes PPM1D, TP53, the regulatory tyrosine kinase JAK2, or mRNA spliceosome components SF3B1, and SRSF2. CHIP is associated with a pro-inflammatory state that has been linked to coronary artery disease, myocardial infarction, and venous thromboembolic disease, as well as prognosis among those with aortic stenosis and heart failure. Heritable and acquired risk factors are associated with increased CHIP prevalence, including germline variation, age, unhealthy lifestyle behaviors (i.e. smoking, obesity), inflammatory conditions, premature menopause, HIV and exposure to cancer therapies. This review aims to summarize emerging research on CHIP, the mechanisms underlying its important role in propagating inflammation and accelerating cardiovascular disease, and new studies detailing the role of associated risk factors and co-morbidities that increase CHIP prevalence.

不确定潜能的克隆性造血 (CHIP) 是由个体的白血病基因突变引起的克隆扩增的造血干细胞的存在，没有血液恶性肿瘤、发育异常或血细胞减少的证据。CHIP 与每年 0.5-1.0% 的白血病风险相关。值得注意的是，它使心血管风险增加两倍，而不受传统风险因素的影响。大约 80% 的 CHIP 患者在表观遗传调节因子DNMT3A、TET2、ASXL1、DNA 损伤修复基因PPM1D、TP53、调节性酪氨酸激酶JAK2或 mRNA 剪接体成分SF3B1和SRSF2中存在突变. CHIP 与促炎状态有关，这种状态与冠状动脉疾病、心肌梗塞和静脉血栓栓塞性疾病以及主动脉瓣狭窄和心力衰竭患者的预后有关。遗传和获得性风险因素与 CHIP 患病率增加有关，包括种系变异、年龄、不健康的生活方式（即吸烟、肥胖）、炎症、过早绝经、HIV 和接受癌症治疗。本综述旨在总结有关 CHIP 的新兴研究、其在传播炎症和加速心血管疾病中重要作用的潜在机制，以及详细说明增加 CHIP 患病率的相关风险因素和合并症的作用的新研究。