Department of Urology, Fundação Antônio Prudente, A.C. Camargo Cancer Center, São Paulo, Brazil.
Department of Pathological Anatomy, Fundação Antônio Prudente, A.C. Camargo Cancer Center, Rua Prof. Antônio Prudente, São Paulo, 211, Brazil.
Curr Urol Rep. 2023 Jul;24(7):345-353. doi: 10.1007/s11934-023-01160-x. Epub 2023 Apr 19.
The physiological aspects of renin-angiotensin system (RAS) components are described in this review. Additionally, we present the main results of studies that could indicate an association between alterations in these components and cancer, particularly renal cell carcinoma (RCC).
The RAS undergoes a series of homeostatic and modulatory processes that extend to hypertrophy, hyperplasia, fibrosis, and remodeling, as well as angiogenesis, pro-inflammatory responses, cell differentiation, stem cell programming, and hematopoiesis. The link between cancer-related inflammation and RAS signaling converge in the response to tumor hypoxia and oxidative stress mechanisms, particularly with the angiotensin type 1 receptor leading to activation of transcription factors such as nuclear factor κB (NF-κB), as well as members of the signal transducer and activation of transcription (STAT) family and HIF1⍺. Dysregulation of the physiological actions of RAS in the microenvironment of inflammation and angiogenesis promotes tumor cell growth.
本文描述了肾素-血管紧张素系统 (RAS) 成分的生理学方面。此外，我们还介绍了这些成分的改变与癌症，特别是肾细胞癌 (RCC) 之间存在关联的主要研究结果。
RAS 经历了一系列的动态平衡和调节过程，这些过程延伸到肥大、增生、纤维化和重塑，以及血管生成、促炎反应、细胞分化、干细胞编程和造血。癌症相关炎症与 RAS 信号之间的联系集中在对肿瘤缺氧和氧化应激机制的反应上，特别是血管紧张素 1 型受体导致转录因子如核因子 κB (NF-κB) 的激活，以及信号转导和转录激活 (STAT) 家族和 HIF1α 的成员。在炎症和血管生成的微环境中，RAS 的生理作用失调会促进肿瘤细胞生长。
