Renin-Angiotensin System Modulation in Oncology
Summary
The renin–angiotensin system (RAS) is increasingly recognised as a multifaceted regulator not only of cardiovascular homeostasis but also of tumour biology. Central to this system are the peptides angiotensin I and angiotensin II, their converting enzymes ACE and ACE2, and their cognate receptors AT1R, AT2R and MasR. In cancer, dysregulation of RAS components can influence cell proliferation, angiogenesis, invasion and the tumour immune microenvironment. Blockade of the ACE/Ang II/AT1R axis by ACE inhibitors or angiotensin receptor blockers has been shown to attenuate mitogenic signalling, reduce new vessel formation and modulate stromal and immune cell function. Conversely, activation of the counter-regulatory ACE2/Ang (1–7)/MasR pathway may exert antitumour effects via induction of apoptosis and suppression of pro-inflammatory mediators. Repurposing RAS-targeting drugs offers a promising strategy to enhance the efficacy of established oncological treatments, mitigate metastasis and overcome resistance mechanisms.
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Renin-Angiotensin System Modulation in Oncology publication trend
The graph below shows the total number of articles in renin-angiotensin system modulation in oncology across all publications each year (not limited to Nature Index journals).
Technical terms
Renin–Angiotensin System (RAS): A hormonal cascade regulating blood pressure and fluid balance, comprising enzymes, peptides and receptors.
Angiotensin II (Ang II): A potent octapeptide effector that binds AT receptors to induce vasoconstriction, cell growth and inflammation.
Angiotensin-Converting Enzyme (ACE): A zinc-dependent dipeptidyl carboxypeptidase that generates Ang II from angiotensin I.
ACE inhibitors (ACEIs): Pharmacological agents that prevent formation of Ang II, thereby attenuating AT1R-mediated signalling.
Angiotensin Receptor Blockers (ARBs): Drugs that selectively antagonise AT1R to inhibit Ang II-driven responses.
AT1 receptor (AT1R): A G-protein-coupled receptor mediating pro-proliferative, pro-angiogenic and pro-inflammatory effects of Ang II.
AT2 receptor (AT2R): A receptor that often counteracts AT1R effects, promoting apoptosis, differentiation and anti-inflammatory actions.
Mas receptor (MasR): A receptor activated by Ang (1–7) that facilitates vasodilation, anti-proliferation and anti-fibrotic pathways.
References
- Effect of renin-angiotensin-aldosterone system inhibitors on survival outcomes in cancer patients treated with immune checkpoint inhibitors: a systematic review and meta-analysis. Frontiers in Immunology (2023).
- The renin-angiotensin-aldosterone system (RAAS) signaling pathways and cancer: foes versus allies. Cancer Cell International (2023).
- Renin-Angiotensin-Aldosterone System Inhibitors and Development of Gynecologic Cancers: A 23 Million Individual Population-Based Study. International Journal of Molecular Sciences (2023).
- The ACE2/Angiotensin-(1–7)/Mas Receptor Axis: Pleiotropic Roles in Cancer. Frontiers in Physiology (2017).
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