Renin-Angiotensin System Interactions in Glioblastoma Therapeutics

Glioblastoma represents the most aggressive primary brain tumour in adults, characterised by rapid proliferation, pervasive invasiveness and profound resistance to conventional therapy. Beyond its classical role in cardiovascular regulation, the renin–angiotensin system (RAS) has emerged as a multifaceted modulator of tumour biology. Components of the RAS are expressed within glioblastoma cell populations, including cancer stem cells, and contribute to angiogenesis, cellular proliferation, hypoxia-driven signalling and remodelling of the tumour microenvironment. Pharmacological agents that target RAS components—such as angiotensin receptor blockers (ARBs) and angiotensin‐converting enzyme inhibitors—are under active investigation for their capacity to impair tumour growth, enhance perfusion and modulate immune infiltration. These repurposed drugs have demonstrated efficacy in preclinical models, reducing vascular density, reprogramming immune landscapes and sensitising tumours to radiotherapy and immunotherapy. Integrative analyses of patient-derived samples and large genomic cohorts have further linked expression of RAS-related genes to survival outcomes and molecular subtypes of glioblastoma. Collectively, these findings underscore the global significance of RAS modulation as a complementary strategy in glioblastoma treatment, offering concrete pathways to translate mechanistic insights into improved clinical protocols.

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Renin-Angiotensin System Interactions in Glioblastoma Therapeutics publication trend

The graph below shows the total number of articles in renin-angiotensin system interactions in glioblastoma therapeutics across all publications each year (not limited to Nature Index journals).

Technical terms

Renin–Angiotensin System: Endocrine cascade involving renin, angiotensin peptides and receptors that regulate blood pressure and tissue homeostasis, implicated in tumour biology.

Angiotensin receptor blockers (ARBs): Pharmaceuticals that inhibit angiotensin II receptors, used to modulate RAS activity and explored for antitumour effects.

Immune checkpoint blockade: Therapeutic approach targeting inhibitory signals on immune cells to enhance antitumour immunity.

Tumour microenvironment: Complex milieu of cancer cells, stromal elements and immune infiltrates that influence tumour growth and therapy response.

Cancer stem cells: Subpopulation of tumour cells with self-renewal capacity and resistance to conventional therapies, driving recurrence.

References

1. Losartan controls immune checkpoint blocker-induced edema and improves survival in glioblastoma mouse models. Proceedings of the National Academy of Sciences of the United States of America (2023).
2. Antiproliferative and apoptotic effects of telmisartan in human glioma cells. Cancer Cell International (2023).
3. Upregulation of the Renin–Angiotensin System Is Associated with Patient Survival and the Tumour Microenvironment in Glioblastoma. Cells (2024).
4. Glioblastoma Multiforme Cancer Stem Cells Express Components of the Renin–Angiotensin System. Frontiers in Surgery (2016).
5. The Renin–Angiotensin System in the Tumor Microenvironment of Glioblastoma. Cancers (2021).