Researchers at the University of Missouri have identified a protein called TG2 in immune cells and blood vessels that may help drive inflammation and arterial changes linked to high blood pressure. Published in the American Journal of Physiology-Heart and Circulatory Physiology, this discovery could pave the way for targeted hypertension therapies.
For nearly half of U.S. adults managing high blood pressure, keeping the condition under control remains a persistent challenge. While there are effective medications out there, many people still struggle to control their hypertension and associated cardiovascular risks. This new research focuses on the molecular pathways connecting immune system regulation, vascular stiffness, and chronic inflammation, opening up possibilities for precision medicine interventions.
In Plain English: The Clinical Takeaway
- The Target: Scientists are investigating a specific protein known as TG2, which is found inside both blood vessel walls and certain immune cells.
- The Mechanism: In experimental models, removing TG2 from myeloid cells—a category of white blood cells involved in inflammation—blunted the rise in blood pressure, arterial stiffness, and inflammation triggered by the hormone angiotensin II.
- The Clinical Goal: Understanding how immune-driven inflammation contributes to hypertension could eventually lead to targeted treatments with potentially fewer side effects.
Cellular Mechanisms of Vascular Stiffening and Inflammation
High blood pressure, or hypertension, increases the risk of heart attacks and strokes. Although the condition has many contributing factors, identifying precise biological drivers allows investigators to look beyond standard management. TG2 was previously linked to arterial stiffening through research on blood vessels. However, the presence of TG2 within immune cells responsible for regulating inflammatory responses prompted a deeper look into its systemic role.
To evaluate this pathway, investigators compared female mice with normal TG2 levels in their myeloid cells against a test group in which TG2 was removed from those exact immune cells. Both groups were administered angiotensin II, a hormone that helps regulate blood pressure. Mice possessing normal TG2 levels demonstrated the expected increases in blood pressure, inflammation, and vascular stiffness. Conversely, those lacking TG2 in their myeloid cells exhibited smaller responses, confirming that the protein contributes to these disease processes.
Translating Experimental Models to Precision Medicine
The experiment points to TG2 activity in myeloid cells as a possible target for reducing inflammation tied to hypertension. However, whether blocking this protein can safely and effectively treat human patients remains to be established. Camila Manrique-Acevedo, an endocrinologist at Harry S. Truman Memorial Veterans’ Hospital and professor at the University of Missouri’s School of Medicine who also treats patients at MU Health Care’s University Hospital, noted the translational objectives of the work. “Tailoring treatments for those who can benefit the most is what precision medicine is all about,” she stated.
Working on the project with Guido Lastra—a School of Medicine associate professor who leads the U.S.-backed study and whose lab investigates TG2—Manrique-Acevedo helped drive the research. Establishing sex-specific differences is a goal before any pharmacological inhibitor targeting TG2 can advance toward human clinical evaluation.
| Research Parameter | Experimental Model Details |
|---|---|
| Target Protein | TG2 found in myeloid and vascular cells. |
| Trigger Agent | Angiotensin II (hormone regulating blood pressure). |
| Observed Effect of TG2 Deletion | Blunted rise in blood pressure, decreased arterial stiffness, and reduced inflammation. |
| Key Investigators | Guido Lastra, Camila Manrique-Acevedo, Huina Niu, and Emma Teixeira. |
| Publishing Journal | American Journal of Physiology-Heart and Circulatory Physiology. |
Contraindications & When to Consult a Doctor
Patients diagnosed with hypertension must never alter, discontinue, or initiate pharmacological regimens without direct consultation with a qualified physician or cardiologist.
References
- Niu, H., Teixeira, E., Manrique-Acevedo, C., & Lastra, G. (2026). Myeloid transglutaminase 2 regulates Treg-Th17 balance in a female model of angiotensin II-induced hypertension and vascular stiffening. American Journal of Physiology-Heart and Circulatory Physiology. DOI: 10.1152/ajpheart.00095.2026
Disclaimer: This article is for informational purposes only and does not constitute medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions regarding a medical condition.
