D'Amato Andrea, Cestiè Claudia, Ferranti Federico, Segato Camilla, Prosperi Silvia, Germanò Rosanna, Myftari Vincenzo, Bartimoccia Simona, Castellani Valentina, Badagliacca Roberto, Cammisotto Vittoria, Pignatelli Pasquale, Vizza Carmine Dario, Severino Paolo
Department of Clinical, Internal, Anesthesiology and Cardiovascular Sciences, Sapienza University of Rome, Viale del Policlinico 155, 00161 Rome, Italy.
Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University, 04100 Latina, Italy.
Int J Mol Sci. 2025 May 28;26(11):5165. doi: 10.3390/ijms26115165.
Heart failure (HF) is a major socioeconomic problem worldwide, associated with high morbidity and mortality due to several underlying diseases. HF is driven by several closely linked mechanisms whose effects are mutually reinforcing. Some of the signalling pathways involved in the progression of HF may initially be compensatory, such as the renin-angiotensin-aldosterone system (RAAS), whose hyperactivation plays a central role in the progression of HF by promoting fluid retention, inflammation, oxidative stress (OS), and myocardial dysfunction. Fluid retention is also promoted by the action of neprilysin, which contrasts natriuresis and vasodilation. Among the compensatory and subsequently maladaptive systems, chronic hyperactivation of the sympathetic nervous system (SNS) exacerbates maladaptive remodelling and drives the progression of HF. At the molecular level, mitochondrial dysfunction and inflammatory substances are involved in the development of a state of systemic oxidative stress and inflammation. The aim of the following manuscript was to revise the pathophysiology and role of OS in HF, focusing on the current knowledge of the molecular pathways involved.
心力衰竭（HF）是一个全球性的重大社会经济问题，与多种基础疾病导致的高发病率和高死亡率相关。HF由几种紧密相连、相互作用的机制驱动。一些参与HF进展的信号通路最初可能具有代偿作用，如肾素-血管紧张素-醛固酮系统（RAAS），其过度激活通过促进液体潴留、炎症、氧化应激（OS）和心肌功能障碍在HF进展中起核心作用。中性肽链内切酶的作用也会促进液体潴留，它与利钠和血管舒张作用相反。在代偿性及随后的适应不良系统中，交感神经系统（SNS）的慢性过度激活会加剧适应不良性重塑并推动HF的进展。在分子水平上，线粒体功能障碍和炎症物质参与了全身氧化应激和炎症状态的发展。以下手稿的目的是修订OS在HF中的病理生理学和作用，重点关注所涉及分子途径的当前知识。
