Hematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, 415 Lane Road, PO Box 801394, Suite 1010, Charlottesville, VA 22908, USA; Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan.65 Tsurumai-cho, Showa-ku, Nagoya 466-8550, Japan.
Hematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, 415 Lane Road, PO Box 801394, Suite 1010, Charlottesville, VA 22908, USA.
Heart Fail Clin. 2022 Jul;18(3):349-359. doi: 10.1016/j.hfc.2022.02.010.
Clonal hematopoiesis is a precancerous state that is recognized as a new causal risk factor for cardiovascular disease. Therapy-related clonal hematopoiesis is a condition that is often found in cancer survivors. These clonal expansions are caused by mutations in DNA damage-response pathway genes that allow hematopoietic stem cells to undergo positive selection in response to the genotoxic stress. These mutant cells increasingly give rise to progeny leukocytes that display enhanced proinflammatory properties. Recent experimental studies suggest that therapy-related clonal hematopoiesis may contribute to the medium- to long-term risk of genotoxic therapies on the cardiovascular system.
克隆性造血是一种癌前状态,被认为是心血管疾病的一个新的因果风险因素。治疗相关的克隆性造血是一种常见于癌症幸存者的情况。这些克隆扩增是由 DNA 损伤反应途径基因突变引起的,这些突变使造血干细胞能够对遗传毒性应激产生阳性选择。这些突变细胞越来越多地产生表现出增强的促炎特性的祖细胞白细胞。最近的实验研究表明,治疗相关的克隆性造血可能导致遗传毒性治疗对心血管系统的中-长期风险增加。