Jin Chenyang, Zhong Zikan, Gao Longzhe, Wu Xiaoyu, Zhou Changzuan, Zhou Genqing, Liu Shaowen
Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, 201620 Shanghai, China.
Rev Cardiovasc Med. 2024 Mar 25;25(4):110. doi: 10.31083/j.rcm2504110. eCollection 2024 Apr.
In this comprehensive review, we examine the intricate interplay between inflammation, ferroptosis, and atrial fibrillation (AF), highlighting their significant roles in AF pathophysiology and pathogenesis. Augmented inflammatory responses are pivotal to AF, potentially leading to atrial remodeling and reentry phenomena by impacting calcium channels and atrial tissue fibrosis. A strong correlation exists between inflammatory cytokines and AF, underscoring the importance of inflammatory signaling pathways, such as NOD-like receptor thermal protien domain associated protein 3 (NLRP3) inflammasome, Nuclear Factor kappa B (NF- B) signaling, and Tumor necrosis factor- (TNF- ) signaling in AF development. Ferroptosis, a non-apoptotic regulated mode of cell death, has been widely studied in relation to cardiovascular diseases including heart failure, myocardial infarction, cardiomyopathy, and reperfusion injury. The interaction between ferroptosis and inflammation is complex and mutually influential. While significant progress has been made in understanding the inflammation-AF relationship, the role of inflammation as a conduit linking ferroptosis and AF remains underexplored. The specific pathogenesis and key molecules of atrial fibrosis caused by ferroptosis are still not fully understood. Here we review the role of inflammatory signaling in ferroptosis and AF. We elucidated the association between ferroptosis and AF, aiming to unveil mechanisms for targeted inhibition of atrial cell fibrosis and to propose novel therapeutic strategies for AF. This exploration is vital for advancing our knowledge and developing more effective interventions for AF, a condition deeply intertwined with inflammatory processes and ferroptotic pathways.
在这篇综述中，我们研究了炎症、铁死亡与心房颤动（AF）之间复杂的相互作用，强调了它们在AF病理生理学和发病机制中的重要作用。增强的炎症反应对AF至关重要，可能通过影响钙通道和心房组织纤维化导致心房重构和折返现象。炎症细胞因子与AF之间存在密切关联，凸显了炎症信号通路在AF发生发展中的重要性，如NOD样受体热蛋白结构域相关蛋白3（NLRP3）炎性小体、核因子κB（NF-κB）信号通路和肿瘤坏死因子-α（TNF-α）信号通路。铁死亡是一种非凋亡性的细胞死亡调控模式，已在包括心力衰竭、心肌梗死、心肌病和再灌注损伤在内的心血管疾病中得到广泛研究。铁死亡与炎症之间的相互作用复杂且相互影响。虽然在理解炎症与AF的关系方面取得了重大进展，但炎症作为连接铁死亡和AF的桥梁的作用仍未得到充分探索。铁死亡导致心房纤维化的具体发病机制和关键分子仍未完全明确。在此，我们综述炎症信号在铁死亡和AF中的作用。我们阐明了铁死亡与AF之间的关联，旨在揭示靶向抑制心房细胞纤维化的机制，并为AF提出新的治疗策略。这一探索对于增进我们对AF的认识以及开发更有效的干预措施至关重要，AF与炎症过程和铁死亡途径密切相关。
