Magnesium inside heart cell mitochondria and how it affects damage after blood flow returns
Official title: Mitochondrial magnesium regulates MCU activity and PTP opening during ischemic reperfusion injury
Funded at Rowan University School/osteopathic Med · NIH-11261579 · Data updated 2026-11-12
This work looks at how magnesium inside heart cell powerhouses affects cell damage when blood flow returns after a heart attack, with the goal of helping people with ischemic heart injury.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Rowan University School/osteopathic Med NIH-funded |
| Lab location | 1 site (Stratford, United States) |
| Project start | January 20, 2025 |
| Project end | November 30, 2029 |
| Funding year | 2026 |
| Award (this year) | $385,000 |
| NIH project number | 5R01HL176747-02 |
| Project ID | NIH-11261579 on NIH RePORTER |
Who could benefit from this research
✓Could help
People who have had a heart attack, are undergoing procedures to restore blood flow (such as angioplasty), or are at risk of ischemia-reperfusion injury would be most relevant to this research.
✕Less likely to help
People without ischemic heart disease or whose heart problems are unrelated to mitochondrial magnesium and calcium handling are unlikely to benefit directly from this work.
What this research studies
This research examines how magnesium inside the mitochondria — the energy centers of heart cells — controls calcium entry and the opening of a pore that can trigger cell death after blood flow is restored. Researchers focus on the Mrs2 protein that brings magnesium into mitochondria and how oxidation during low-oxygen and reoxygenation stress impairs its function. Using lab-grown heart cells and molecular experiments, they measure magnesium and calcium levels, mitochondrial function, and cell survival to link impaired magnesium influx to reperfusion injury. The results may point to ways to preserve mitochondrial magnesium and protect heart cells during treatments that restore blood flow.
Why it matters
Potential benefit: If successful, this work could point to new treatments that protect heart cells from damage after heart attacks by preserving mitochondrial magnesium and preventing calcium-triggered cell death.
How similar studies have gone: Previous lab and animal studies support roles for magnesium and mitochondrial calcium in cell survival, but linking Mrs2 oxidation to reperfusion injury is a novel mechanism being explored.
Where this research is happening
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Rowan University School/osteopathic Med
Stratford, United States Active
Researchers
- Principal investigator: Santhanam, Shanmughapriya — Rowan University School/osteopathic Med
- Study coordinator: Santhanam, Shanmughapriya
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.