Kallikourdis Marinos, Cochran Jesse D, Walsh Kenneth, Condorelli Gianluigi
Department of Biomedical Sciences, Humanitas University, Pieve Emanuele (MI), Italy (M.K., G.C.).
Department of Cardiovascular Medicine, IRCCS Humanitas Research Hospital, Rozzano (MI), Italy (M.K., G.C.).
Circ Res. 2025 May 23;136(11):1208-1232. doi: 10.1161/CIRCRESAHA.125.325489. Epub 2025 May 22.
Heart failure is the final outcome of most cardiovascular diseases and shares risk factors with other cardiovascular pathologies. Among these, inflammation plays a central role in disease progression and myocardial remodeling. Over the past 2 decades, numerous studies have explored immune-related mechanisms in cardiovascular disease, highlighting the importance of immune cross-talk between the heart and extra-cardiac organs, including bone marrow, spleen, liver, gut, and adipose tissue. This review examines how immune interactions among these organs contribute to heart failure pathogenesis, with a focus on clonal hematopoiesis, an age-related alteration of hematopoietic stem cells that fosters pathological bone marrow-heart communication. Additionally, we explore recent advances in the understanding of clonal hematopoiesis and its role in heart failure, emphasizing its implications for prognosis and potential therapeutic interventions. By integrating insights from immunology, metabolism, and aging, we provide a comprehensive perspective on the immunologic determinants of heart failure, paving the way for precision medicine approaches aimed at mitigating cardiovascular risk.
心力衰竭是大多数心血管疾病的最终结局，且与其他心血管疾病共享风险因素。其中，炎症在疾病进展和心肌重塑中起核心作用。在过去20年里，大量研究探索了心血管疾病中与免疫相关的机制，突显了心脏与心外器官（包括骨髓、脾脏、肝脏、肠道和脂肪组织）之间免疫相互作用的重要性。本综述探讨了这些器官之间的免疫相互作用如何促成心力衰竭的发病机制，重点关注克隆性造血，这是一种与年龄相关的造血干细胞改变，促进了病理性骨髓-心脏通讯。此外，我们探讨了对克隆性造血及其在心力衰竭中作用的最新认识进展，强调其对预后的影响以及潜在的治疗干预措施。通过整合来自免疫学、代谢学和衰老研究的见解，我们提供了关于心力衰竭免疫决定因素的全面观点，为旨在降低心血管风险的精准医学方法铺平了道路。
