How kidneys get injured and heal after sudden damage
Mechanisms of Ischemic Kidney Injury and Repair
['FUNDING_R01'] · BRIGHAM AND WOMEN'S HOSPITAL · NIH-11257357
This work looks at how kidney tubule cells react to sudden injury and explores ways to stop scarring and long-term kidney damage for people with acute kidney injury.
Quick facts
| Phase | ['FUNDING_R01'] |
|---|---|
| Study type | Nih_funding |
| Sex | All |
| Sponsor | BRIGHAM AND WOMEN'S HOSPITAL (nih funded) |
| Locations | 1 site (BOSTON, UNITED STATES) |
| Trial ID | NIH-11257357 on ClinicalTrials.gov |
What this research studies
From a patient point of view, researchers are studying the cells in the kidney that are first hurt during sudden (ischemic) injury and how those cells either recover or trigger scarring. They use genetically modified mice, including animals with specific genes turned off in tubule cells and a special mouse that can be made to have DNA damage, to mimic different types of kidney injury. The team is focusing on DNA-damage signals (like BRCA1, BRD4, and lamin A) and how injured tubule cells release factors that turn nearby support cells into scar-forming myofibroblasts. They also test drugs that might block these pathways to prevent the harmful scarring that leads to chronic kidney problems.
Who could benefit from this research
Good fit: People who have recently had acute kidney injury (for example from low blood flow, blockage, or certain toxins) or who are at high risk for ischemic kidney damage would be the most relevant patients for the findings and any future trials.
Not a fit: Patients whose kidney disease is due to genetic disorders or non-ischemic causes that do not involve proximal tubule injury may not benefit from these specific approaches.
Why it matters
Potential benefit: If successful, this work could point to new treatments that prevent scarring after acute kidney injury and reduce the chance of developing long-term kidney disease.
How similar studies have performed: Previous animal studies have linked DNA damage and cellular senescence to kidney fibrosis, but targeting the BRCA1/BRD4/lamin A pathway and the COUP-TFII-driven fibroblast activation is a more novel therapeutic angle.
Where this research is happening
BOSTON, UNITED STATES
- BRIGHAM AND WOMEN'S HOSPITAL — BOSTON, UNITED STATES (ACTIVE)
Researchers
- Principal investigator: BONVENTRE, JOSEPH VINCENT — BRIGHAM AND WOMEN'S HOSPITAL
- Study coordinator: BONVENTRE, JOSEPH VINCENT
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.