Shi Shuqing, Zhang Bingxuan, Li Yumeng, Xu Xia, Lv Jiayu, Jia Qiulei, Chai Ruoning, Xue Wenjing, Li Yuan, Wang Yajiao, Wu Huaqin, Song Qingqiao, Hu Yuanhui
Department of Internal Medicine, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Beijing University of Chinese Medicine, Beijing, China.
Front Cardiovasc Med. 2022 Feb 25;9:837270. doi: 10.3389/fcvm.2022.837270. eCollection 2022.
The crosstalk between the heart and kidney is carried out through various bidirectional pathways. Cardiorenal syndrome (CRS) is a pathological condition in which acute or chronic dysfunction in the heart or kidneys induces acute or chronic dysfunction of the other organ. Complex hemodynamic factors and biochemical and hormonal pathways contribute to the development of CRS. In addition to playing a critical role in generating metabolic energy in eukaryotic cells and serving as signaling hubs during several vital processes, mitochondria rapidly sense and respond to a wide range of stress stimuli in the external environment. Impaired adaptive responses ultimately lead to mitochondrial dysfunction, inducing cell death and tissue damage. Subsequently, these changes result in organ failure and trigger a vicious cycle. and animal studies have identified an important role of mitochondrial dysfunction in heart failure (HF) and chronic kidney disease (CKD). Maintaining mitochondrial homeostasis may be a promising therapeutic strategy to interrupt the vicious cycle between HF and acute kidney injury (AKI)/CKD. In this review, we hypothesize that mitochondrial dysfunction may also play a central role in the development and progression of CRS. We first focus on the role of mitochondrial dysfunction in the pathophysiology of HF and AKI/CKD, then discuss the current research evidence supporting that mitochondrial dysfunction is involved in various types of CRS.
心脏与肾脏之间的相互作用通过多种双向途径进行。心肾综合征（CRS）是一种病理状态，其中心脏或肾脏的急性或慢性功能障碍会诱发另一器官的急性或慢性功能障碍。复杂的血流动力学因素以及生化和激素途径促成了CRS的发展。线粒体除了在真核细胞中产生代谢能量以及在多个重要过程中充当信号枢纽方面发挥关键作用外，还能快速感知并响应外部环境中的多种应激刺激。适应性反应受损最终会导致线粒体功能障碍，引发细胞死亡和组织损伤。随后，这些变化会导致器官衰竭并触发恶性循环。动物研究已证实线粒体功能障碍在心力衰竭（HF）和慢性肾脏病（CKD）中起重要作用。维持线粒体稳态可能是中断HF与急性肾损伤（AKI）/CKD之间恶性循环的一种有前景的治疗策略。在本综述中，我们推测线粒体功能障碍可能在CRS的发生和发展中也起核心作用。我们首先关注线粒体功能障碍在HF和AKI/CKD病理生理学中的作用，然后讨论支持线粒体功能障碍参与各种类型CRS的当前研究证据。
