NIH-funded research R01 grant

Role of LKB1 in reduced lung blood vessel growth in BPD

Official title: Role of Liver Kinase B1 in the decreased angiogenesis in bronchopulmonary dysplasia

Funded at Medical College of Wisconsin · NIH-11378318 · Data updated 2026-11-12

Aims to understand how a cellular regulator (LKB1) affects blood vessel formation in the lungs of preterm infants at risk for bronchopulmonary dysplasia.

More Bronchopulmonary Dysplasia research and trials

Quick facts

Grant typeR01 grant
Study typeNIH-funded research
Funding institutionMedical College of Wisconsin
NIH-funded
Lab location1 site (Milwaukee, United States)
Project startJuly 15, 2024
Project endJune 30, 2028
Funding year2026
Award (this year)$632,540
NIH project number5R01HL174635-03
Project IDNIH-11378318 on NIH RePORTER

Who could benefit from this research

Could help

Infants at risk for or diagnosed with bronchopulmonary dysplasia, particularly those with oxygen exposure history.

Less likely to help

Very premature infants without BPD or those not exposed to hyperoxia may see no direct benefit.

What this research studies

Bronchopulmonary dysplasia is a common problem in babies born early and is worsened by high oxygen exposure. This grant studies how reduced LKB1 and related AMPK signaling in lung endothelial cells may limit new blood vessel growth, contributing to BPD. Using neonatal mouse models, the researchers will explore how LKB1, AMPK, and mitochondrial biogenesis interact to drive angiogenesis in the lungs and whether activating AMPK can restore normal vessel formation. The work builds on prior findings that metformin can improve mitochondrial function and lung angiogenesis in hyperoxia, with the goal of translating these insights toward human therapies. Overall, the project seeks to map the molecular pathway from cellular energy sensing to blood vessel growth in the developing lung to inform future treatments for BPD.

Why it matters

Potential benefit: If successful, the findings could guide new therapies to promote lung blood vessel growth and reduce BPD severity in preterm infants.

How similar studies have gone: Previous studies showed that activating AMPK pathways can improve mitochondrial function and angiogenesis in experimental lung models, supporting this approach.

Where this research is happening

  • Medical College of Wisconsin
    Milwaukee, United States
    Active

Researchers

  • Principal investigator: Konduri, Girija G. — Medical College of Wisconsin
  • Study coordinator: Konduri, Girija G.

Related research

Other NIH-funded projects on the same topics.

About this research

  1. This is an active NIH-funded research project — typically early-stage science, not a clinical trial accepting patient enrollment.
  2. Some NIH-funded labs run parallel clinical studies or seek volunteers for related work. To check, contact the principal investigator or institution listed above.
  3. For full project details, budget, and progress reports, visit the official NIH RePORTER page.
Last reviewed 2026-11-14 by the Find a Trial editorial team. Information on this page is for educational purposes and is not medical advice. Always consult qualified healthcare professionals about clinical trial participation.