Riehle C, Bauersachs J
Department of Cardiology and Angiology, Hannover Medical School, Carl-Neuberg-Str. 1, 30625, Hannover, Germany.
Herz. 2019 Apr;44(2):96-106. doi: 10.1007/s00059-019-4785-8.
Inflammation plays a central role in the development of heart failure, especially in heart failure with preserved ejection fraction (HFpEF). Furthermore, the inflammatory response enables the induction of regenerative processes following acute myocardial injury. Recent studies in humans and animals have greatly advanced our understanding of the underlying mechanisms behind these adaptations. Importantly, inflammation can have both beneficial and detrimental effects, dependent on its extent, localization, and duration. Therefore, modulation of cardiac inflammation has been suggested as an attractive target for the treatment of heart failure, which has been investigated in numerous clinical trials. This review discusses key inflammatory mechanisms contributing to the pathogenesis of heart failure and their potential impact as therapeutic targets.
炎症在心力衰竭的发生发展中起着核心作用，尤其是在射血分数保留的心力衰竭（HFpEF）中。此外，炎症反应能够在急性心肌损伤后诱导再生过程。最近在人类和动物身上进行的研究极大地推进了我们对这些适应性变化背后潜在机制的理解。重要的是，炎症根据其程度、部位和持续时间可产生有益和有害两种影响。因此，调节心脏炎症已被认为是治疗心力衰竭的一个有吸引力的靶点，并且已经在众多临床试验中进行了研究。本综述讨论了导致心力衰竭发病机制的关键炎症机制及其作为治疗靶点的潜在影响。
