How heart attacks and oxidative stress damage the heart's calcium release channel
Official title: New mechanisms of cardiac ryanodine receptor dysfunction during oxidative stress: the role of intersubunit cross-linking
Funded at Loyola University Chicago · NIH-11264827 · Data updated 2026-11-12
Researchers will see if specific chemical bonds form between parts of the heart's calcium release channel during oxidative damage from a heart attack and cause calcium imbalance that leads to poor heart contractions and arrhythmias.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Loyola University Chicago NIH-funded |
| Lab location | 1 site (Maywood, United States) |
| Project start | February 1, 2025 |
| Project end | November 30, 2028 |
| Funding year | 2026 |
| Award (this year) | $621,499 |
| NIH project number | 5R01HL176568-02 |
| Project ID | NIH-11264827 on NIH RePORTER |
Who could benefit from this research
✓Could help
People who have had a myocardial infarction or who are at high risk for ischemic heart disease would be the most relevant group for future therapies arising from this work.
✕Less likely to help
Patients with heart problems unrelated to ischemia-driven ryanodine receptor dysfunction or those seeking immediate clinical treatments will not directly benefit from this basic research.
What this research studies
This project uses a specially engineered mouse model that carries a human-like change in the heart's ryanodine receptor protein. Scientists will expose heart tissue to oxidative stress and mimic heart attacks to observe whether disulfide bonds form between receptor subunits and how that changes calcium release. They will measure heart cell calcium handling and electrical activity, identify the precise cysteine sites involved in intersubunit cross-linking, and test whether preventing those links restores normal function. Results will guide whether drugs or other therapies that block this cross-linking might help people after myocardial infarction.
Why it matters
Potential benefit: If confirmed, this could identify new targets for therapies to prevent calcium imbalance, reduce arrhythmias, and improve recovery after heart attacks.
How similar studies have gone: Prior laboratory work supports the idea that oxidative cross-linking can activate the ryanodine receptor, but translating this mechanism into patient treatments is still novel and unproven.
Where this research is happening
-
Loyola University Chicago
Maywood, United States Active
Researchers
- Principal investigator: Zima, Aleksey V — Loyola University Chicago
- Study coordinator: Zima, Aleksey V
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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.