Abstract
The renin-angiotensin system (RAS) is an important signaling system within the tumor microenvironment, promoting both malignant and stromal cell proliferation. Angiotensin II (AngII) is the main effector hormone, acting predominantly by the signaling of angiotensin II type 1 receptor (AT1R). Preclinical data show that AngII increases TGF-β production through AT1R signaling and decreases TGF-β through AT2R signaling. Thus, the overlap of these pathways may have a critical role in carcinogenesis, as well as immune evasion and inhibiting AT1R may enhance clinical responses in combination with immune checkpoint inhibitors (ICI).
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
