How immune signals may cause high blood pressure in women with autoimmune disease
Innate Immune Mediated Changes in Renal Function to Cause Hypertension in Females with Autoimmune Disease
This project looks at whether innate immune signals cause kidney changes that raise blood pressure in women with autoimmune disease like lupus.
Quick facts
| Grant type | NIH-funded research |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Augusta University NIH-funded |
| Lab location | 1 site (Augusta, United States) |
| Project ID | NIH-11180421 on NIH RePORTER |
What this research studies
This work uses a female mouse model of systemic lupus erythematosus to study how innate immune activity affects the kidneys and blood pressure. Researchers will measure oxidative stress, neutrophil extracellular traps (NETs), and stress signals such as HMGB1 and TLR4, and examine how these change kidney blood flow and sodium handling. They will test whether interrupting those immune and oxidative pathways improves renal function and lowers blood pressure in the model. Findings are intended to guide future research aimed at helping women with autoimmune-driven hypertension.
Who could benefit from this research
Good fit: Women with autoimmune diseases—especially systemic lupus erythematosus (SLE)—who also have high blood pressure would be the most relevant group for this work.
Not a fit: People without autoimmune disease or whose hypertension is due to unrelated causes may not benefit from these findings.
Why it matters
Potential benefit: If successful, this could point to new treatments that target immune signaling or oxidative stress to lower blood pressure in women with autoimmune disease.
How similar studies have performed: Prior mouse studies showed antioxidants can reduce hypertension in lupus models, but the specific innate immune–ROS–kidney feedforward mechanism tested here is largely novel.
Where this research is happening
Augusta, United States
- Augusta University — Augusta, United States (Active)
Researchers
- Principal investigator: Ryan, Michael — Augusta University
- Study coordinator: Ryan, Michael
About this research
- This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
- Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
- For full project details, budget, and progress reports, visit the official NIH RePORTER page below.