Abstract:
Improvements in therapies for heart failure with preserved ejection fraction (HFpEF) are crucial for improving patient outcomes and quality of life. Although HFpEF is the predominant heart failure type among older individuals, its prognosis is often poor owing to the lack of effective therapies. The roles of the spleen and bone marrow are often overlooked in the context of HFpEF. Recent studies suggest that the spleen and bone marrow could play key roles in HFpEF, especially in relation to inflammation and immune responses. The bone marrow can increase production of certain immune cells that can migrate to the heart and contribute to disease. The spleen can contribute to immune responses that either protect or exacerbate heart failure. Extramedullary hematopoiesis in the spleen could play a crucial role in HFpEF. Increased metabolic activity in the spleen, immune cell production and mobilization to the heart, and concomitant cytokine production may occur in heart failure. This leads to systemic chronic inflammation, along with an imbalance of immune cells (macrophages) in the heart, resulting in chronic inflammation and progressive fibrosis, potentially leading to decreased cardiac function. The bone marrow and spleen are involved in altered iron metabolism and anemia, which also contribute to HFpEF. This review presents the concept of an interplay between the heart, spleen, and bone marrow in the setting of HFpEF, with a particular focus on extramedullary hematopoiesis in the spleen. The aim of this review is to discern whether the spleen can serve as a new therapeutic target for HFpEF.
摘要:
改善射血分数保留的心力衰竭(HFpEF)的治疗方法对于改善患者预后和生活质量至关重要。尽管HFpEF是老年人中主要的心力衰竭类型,由于缺乏有效的治疗方法,其预后通常较差。在HFpEF的背景下,脾和骨髓的作用经常被忽视。最近的研究表明,脾和骨髓可能在HFpEF中起关键作用,尤其是与炎症和免疫反应有关。骨髓可以增加某些免疫细胞的产生,这些免疫细胞可以迁移到心脏并导致疾病。脾脏可以促进保护或加剧心力衰竭的免疫反应。脾脏的髓外造血在HFpEF中起着至关重要的作用。脾脏的代谢活动增加,免疫细胞产生和动员到心脏,和伴随细胞因子的产生可能发生在心力衰竭。这导致全身性慢性炎症,伴随着心脏中免疫细胞(巨噬细胞)的失衡,导致慢性炎症和进行性纤维化,可能导致心脏功能下降。骨髓和脾脏参与铁代谢改变和贫血,这也有助于HFpEF。这篇综述提出了心之间相互作用的概念,脾,脾和骨髓在HFpEF的情况下,特别关注脾脏的髓外造血。这篇综述的目的是辨别脾脏是否可以作为HFpEF的新治疗靶标。