Chiuariu Traian, Șalaru Delia, Ureche Carina, Vasiliu Laura, Lupu Ancuta, Lupu Vasile Valeriu, Șerban Adela Mihaela, Zăvoi Alexandra, Benchea Laura Catalina, Clement Alexandra, Tudurachi Bogdan-Sorin, Sascău Radu Andy, Stătescu Cristian
Department of Internal Medicine, Faculty of Medicine, Grigore T. Popa University of Medicine and Pharmacy of Iasi, 16 University Street, 700115 Iasi, Romania.
Prof. Dr. George I.M. Georgescu Institute of Cardiovascular Diseases, Carol I Boulevard, No. 50, 700503 Iasi, Romania.
J Cardiovasc Dev Dis. 2024 Feb 16;11(2):62. doi: 10.3390/jcdd11020062.
Cardiovascular disease (CVD) and chronic kidney disease (CKD) often coexist and have a major impact on patient prognosis. Organ fibrosis plays a significant role in the pathogenesis of cardio-renal syndrome (CRS), explaining the high incidence of heart failure and sudden cardiac death in these patients. Various mediators and mechanisms have been proposed as contributors to the alteration of fibroblasts and collagen turnover, varying from hemodynamic changes to the activation of the renin-angiotensin system, involvement of FGF 23, and Klotho protein or collagen deposition. A better understanding of all the mechanisms involved has prompted the search for alternative therapeutic targets, such as novel inhibitors of the renin-angiotensin-aldosterone system (RAAS), serelaxin, and neutralizing interleukin-11 (IL-11) antibodies. This review focuses on the molecular mechanisms of cardiac and renal fibrosis in the CKD and heart failure (HF) population and highlights the therapeutic alternatives designed to target the responsible pathways.
心血管疾病(CVD)和慢性肾脏病(CKD)常并存,对患者预后有重大影响。器官纤维化在心肾综合征(CRS)的发病机制中起重要作用,这解释了这些患者心力衰竭和心源性猝死的高发生率。各种介质和机制已被提出是成纤维细胞和胶原蛋白更新改变的促成因素,从血流动力学变化到肾素 - 血管紧张素系统的激活、FGF 23的参与、Klotho蛋白或胶原蛋白沉积等。对所有相关机制的更好理解促使人们寻找替代治疗靶点,如肾素 - 血管紧张素 - 醛固酮系统(RAAS)的新型抑制剂、松弛素和中和白细胞介素 - 11(IL - 11)抗体。本综述重点关注CKD和心力衰竭(HF)人群中心脏和肾脏纤维化的分子机制,并强调旨在针对相关途径的治疗选择。