How kidney blood-vessel cells sense low oxygen after sudden kidney injury
Endothelial oxygen sensing and metabolic reprogramming in AKI to CKD transition
This work looks at whether changes in oxygen sensing and metabolism in kidney blood-vessel cells after sudden (ischemic) kidney injury lead to scarring and long-term kidney disease, with the goal of helping people who have had acute kidney injury.
Quick facts
| Grant type | R01 grant |
|---|---|
| Study type | NIH-funded research |
| Funding institution | Northwestern University NIH-funded |
| Lab location | 1 site (Chicago, United States) |
| Project ID | NIH-11141892 on NIH RePORTER |
What this research studies
Researchers use a mix of mouse models and human kidney tissue to follow how endothelial (blood-vessel) cells respond to low oxygen after ischemic acute kidney injury. They apply genetic tools and single-cell RNA sequencing to map which oxygen-sensing enzymes (PHD1-3) and metabolic pathways are turned on in those cells. In preclinical experiments they tested a drug that blocks the lactate exporter MCT4 (syrosingopine) and found it helped the kidney heal without excessive scarring. The team is focusing on endothelial PHD3 as a key regulator and exploring whether targeting these pathways could be turned into new treatments.
Who could benefit from this research
Good fit: People who recently experienced ischemic acute kidney injury or are at high risk of progressing from AKI to CKD would be the most relevant candidates for future related trials.
Not a fit: People with long-standing chronic kidney disease from non-ischemic causes are less likely to benefit from these approaches.
Why it matters
Potential benefit: If successful, this research could point to new therapies that prevent progression from acute kidney injury to chronic kidney disease by targeting endothelial oxygen sensing or lactate transport.
How similar studies have performed: Preclinical work in mice and analyses of human kidney samples have shown promise for targeting endothelial metabolism and MCT4 to reduce fibrosis, but this approach has not yet been tested in patients.
Where this research is happening
Chicago, United States
- Northwestern University — Chicago, United States (Active)
Researchers
- Principal investigator: Kapitsinou, Pinelopi P. — Northwestern University
- Study coordinator: Kapitsinou, Pinelopi P.
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.