Blocking signals that help the Chagas parasite survive in the heart
Official title: Targeting purinergic signaling in Chagas disease
Funded at National Research Council of Argentina · NIH-11317233 · Data updated 2026-11-12
This project looks at whether stopping the signals that turn injury-related ATP into immune-suppressing adenosine could help people with Chagas-related heart disease.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | National Research Council of Argentina NIH-funded |
| Lab location | 1 site (Cordoba, Argentina) |
| Project start | April 1, 2023 |
| Project end | March 31, 2028 |
| Funding year | 2026 |
| Award (this year) | $132,428 |
| NIH project number | 5R01AI176457-04 |
| Project ID | NIH-11317233 on NIH RePORTER |
Who could benefit from this research
✓Could help
People with chronic T. cruzi (Chagas) infection, especially those with early or progressing heart involvement, would be the most relevant candidates for future trials or treatments.
✕Less likely to help
People without Chagas infection or those with very advanced, irreversible heart failure are unlikely to receive direct benefit from immune-targeting approaches.
What this research studies
Researchers are studying how damaged heart cells release ATP that is turned into adenosine, which may weaken immune attack and allow Trypanosoma cruzi to persist in the heart. In laboratory heart cells, animal models, and human heart samples, they will test ways to block the enzymes and pathways that produce adenosine. They will measure how these interventions affect parasite survival, inflammation, and heart muscle function, and how they interact with the existing drug benznidazole. The aim is to find treatment targets that could slow or prevent Chagas cardiomyopathy.
Why it matters
Potential benefit: If successful, this work could point to new treatments that help the immune system clear the parasite and slow or prevent Chagas-related heart damage.
How similar studies have gone: Modulating ATP-to-adenosine signaling has shown promise in other infectious and inflammatory models, but applying this approach to Chagas cardiomyopathy is relatively new and not yet proven in patients.
Where this research is happening
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National Research Council of Argentina
Cordoba, Argentina Active
Researchers
- Principal investigator: Aoki, Maria Pilar — National Research Council of Argentina
- Study coordinator: Aoki, Maria Pilar
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.