In summer 2024, two forward-thinking university students, Martha Old and Rachel Nguyen, were awarded prestigious Summer Studentships by Action for Pulmonary Fibrosis (APF) and the British Association for Lung Research (BALR). Under the expert guidance of Dr. Alison John (Imperial College London) and Dr. Rachel Walters (University College London), they spent eight weeks tackling questions about pulmonary fibrosis (PF).
Both Martha and Rachel explored the role of different proteins in the lungs, RPAP1 and mTOR, in driving lung scarring. Here we take a deeper look at Martha and Rachel’s vital findings.
Martha’s Research:RPAP1—The Stuck Volume Knob
Martha’s research has uncovered how a protein, RPAP1, may drive lung scarring, which could lead to new treatments.
During her project, Martha investigated which cells produce RPAP1 in both healthy and diseased lung tissues. She discovered that RPAP1 levels are higher in lung tissue samples from people with IPF who have more severe disease. Even more fascinating, when healthy lung cells were placed in an environment mimicking diseased lungs, their RPAP1 levels shot up, and they started behaving abnormally.
Imagine RPAP1 as a volume knob controlling the lung’s healing response. In a healthy person, this knob adjusts smoothly in a controlled way, allowing for balanced repair when the lungs face everyday damage from pollution or dust. But in people with a faulty gene, the knob is stuck on maximum, cranking up the repair process so much that it leads to excessive scarring instead of healing. Over time, this makes breathing harder and harder.
.png)
Understanding the consequences of permanently increased RPAP1 levels in the lungs could help identify new ways to either repair the faulty volume knob, cut off its power, or interrupt the signal from the volume knob to the speaker, thereby reducing the scarring process.
What’s Next? Can We Turn the Volume Down?
Martha’s research has sparked new questions about the role of RPAP1 in lung fibrosis.
- Understanding the problem: Figuring out how RPAP1 triggers scarring and how to stop it.
- Testing treatments: Exploring whether any existing drugs could block the protein’s harmful signals or whether new drugs will be required
- Early detection: Developing a blood test to spot the issue early and start treatment before serious lung damage happens.
Martha’s studentship has uncovered key biological processes that drive lung fibrosis. Her work is a step closer to creating targeted treatments to benefit pulmonary fibrosis patients in the future.
Rachel’s Research: mTOR - The Overloaded Control Tower
Rachel’s research shines further light on how a protein, mTOR, drives lung scarring. This could lead to new treatments.
Rachel studied mTOR, a protein that acts like an airport control tower for lung cells, directing plane flight paths, arrivals, and departures. If the control tower allowed planes to keep arriving but not departing, the airport would stop working effectively.
When mTOR becomes too active, this causes lung cells called fibroblasts to ‘misbehave’ by producing too much collagen – which is a major component of scar tissue. Over time this can cause the lungs to become stiffer, making it harder to breathe. Scientists have found that blocking or lowering the activity of mTOR can reduce the build up of scar tissue.
There are some drugs already out there which can lower the activity of mTOR but as it’s a control centre and impacts a lot of different processes, we need to learn more to help us create drugs which target specific pathways regulated by this control centre. This will ensure that new drugs treat fibrosis without disrupting other vital cell functions.
This is why mTOR is an important focus for more research and for developing new treatments to stop or even reverse fibrosis.
What's Next? Fine-Tuning the Control Tower
Rachel’s work brings us closer to understanding how mTOR, the cell’s “control tower” can be adjusted to improve the lives of those living with PF.
Next research steps:
- Targeting scarring: Understanding how mTOR drive the scarring process could help us to stop scarring in its tracks
- Broadening research: Exploring mTOR in different lung cells to understand more about its impact.
- New treatments: Finding new ways to adjust mTOR activity may lead to new and better therapies for PF.
New Opportunities: 2025 BALR Summer Studentships
Building on the success of previous studentships, APF, BALR, Pulmonary Fibrosis Northern Ireland, and Breathing Matters are excited to announce the 2025 BALR Summer Studentships. These studentships provide undergraduate science or medical students the chance to work on 8-week research projects focused on lung diseases like pulmonary fibrosis, asthma, and COPD.
Students will gain hands-on experience in real scientific studies, working alongside experienced researchers. The studentship covers a stipend (financial support), research costs, and travel expenses to present findings at a scientific conference.
Applications are now open and close 10th May 2025. Interested students can visit the BALR website for more details on eligibility and how to apply.
This is a fantastic opportunity for students eager to gain research experience while contributing to advancements in lung disease treatments.
Stay tuned for more updates as we continue to push the boundaries of pulmonary fibrosis research!
This wouldn’t be possible without the incredible generosity of our supporters.
You can help make a difference today:
Donate: Every gift, no matter the size, helps continue our vital work. Your donations fuel progress in research, care, and support for people living with PF.
Sign Up for a Fundraiser: Organise a fundraising activity and contribute to our mission in a fun and meaningful way.