Department of Biochemistry and Environmental Chemistry, George Emil Palade University of Medicine, Pharmacy, Sciences and Technology of Targu Mures, 540142 Targu Mures, Romania.
Department of Cardiology, Clinical County Hospital Mures, 540103 Targu Mures, Romania.
Int J Mol Sci. 2021 Dec 2;22(23):13053. doi: 10.3390/ijms222313053.
Inflammation has emerged as an important contributor to heart failure (HF) development and progression. Current research data highlight the diversity of immune cells, proteins, and signaling pathways involved in the pathogenesis and perpetuation of heart failure. Chronic inflammation is a major cardiovascular risk factor. Proinflammatory signaling molecules in HF initiate vicious cycles altering mitochondrial function and perturbing calcium homeostasis, therefore affecting myocardial contractility. Specific anti-inflammatory treatment represents a novel approach to prevent and slow HF progression. This review provides an update on the putative roles of inflammatory mediators involved in heart failure (tumor necrosis factor-alpha; interleukin 1, 6, 17, 18, 33) and currently available biological and non-biological therapy options targeting the aforementioned mediators and signaling pathways. We also highlight new treatment approaches based on the latest clinical and experimental research.
炎症已成为心力衰竭（HF）发展和进展的重要因素。目前的研究数据强调了参与心力衰竭发病机制和持续存在的免疫细胞、蛋白质和信号通路的多样性。慢性炎症是主要的心血管危险因素。HF 中的促炎信号分子会引发恶性循环，改变线粒体功能并扰乱钙稳态，从而影响心肌收缩力。特定的抗炎治疗代表了预防和减缓 HF 进展的一种新方法。本文综述了参与心力衰竭的炎症介质（肿瘤坏死因子-α；白细胞介素 1、6、17、18、33）的假定作用，以及目前针对上述介质和信号通路的生物和非生物治疗选择，并强调了基于最新临床和实验研究的新治疗方法。
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