How the AMPK energy-sensor affects whether minimal change disease becomes FSGS
Official title: Role of AMP-kinase pathway in the regulation of Minimal change disease-to-FSGS transition
Funded at Yale University · NIH-11235113 · Data updated 2026-11-12
This work looks at how a cell energy sensor called AMPK helps protect kidney filter cells and whether that keeps people with minimal change disease from progressing to focal segmental glomerulosclerosis.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Yale University NIH-funded |
| Lab location | 1 site (New Haven, United States) |
| Project start | December 15, 2022 |
| Project end | November 30, 2027 |
| Funding year | 2026 |
| Award (this year) | $495,830 |
| NIH project number | 5R01DK132274-04 |
| Project ID | NIH-11235113 on NIH RePORTER |
Who could benefit from this research
✓Could help
People diagnosed with minimal change disease, especially those with early signs that could suggest progression toward FSGS, would be the ideal candidates related to this work.
✕Less likely to help
Patients who already have long-standing FSGS with extensive scarring or those with end-stage kidney disease are unlikely to benefit from these early molecular-focused experiments.
What this research studies
Researchers compare kidney tissue from people with minimal change disease (MCD) and FSGS, and use mouse and cell models that mimic MCD-like changes. They change AMPK activity in those models to see how podocyte structure, survival, and scarring are affected. The team studies how loss of a protein called Fyn leads to AMPK shifts and links those molecular changes to what is seen in patient samples. Results will help decide if targeting AMPK could stop MCD from switching into the scarring form FSGS.
Why it matters
Potential benefit: If successful, the findings could point to ways to keep podocytes alive and prevent MCD from progressing to FSGS and eventual kidney failure.
How similar studies have gone: Prior animal and cellular studies have suggested AMPK can protect podocytes and limit hypertrophy, but translating this into human therapies remains novel and unproven.
Where this research is happening
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Yale University
New Haven, United States Active
Researchers
- Principal investigator: Menon, Madhav C — Yale University
- Study coordinator: Menon, Madhav C
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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.