Dr Wenying Lu (aka Monica) is a Research Fellow and Lab Manager at the Respiratory Translational Research Group (RTRG) in the School of Health Sciences at the University of Tasmania.
Please  tell me a about your recent success in the travel grants, what you won for,  where you went and what you gained from the experience?
I was honoured to receive the CREATE Travel Grant, which supported my attendance at the European Respiratory Society (ERS) International Congress 2025 in Amsterdam. In addition, I was awarded the Janet Elder Award 2025 by the Thoracic Society of Australia and New Zealand. These awards recognised my ongoing research into idiopathic pulmonary fibrosis (IPF), focusing on adipose tissue deposition, adipose tissue driven inflammatory mediators, and role of epithelial to mesenchymal transition (EMT) in fibrotic lung disease.
At ERS, I presented my recent findings on how metabolic, and tissue-remodelling intersect in IPF pathogenesis. Attending ERS provided an invaluable opportunity to engage with leading international researchers, make potential collaborations in the field, and gain insights into the latest therapeutic advances and experimental models of  pulmonary fibrosis.
This experience significantly broadened my international research network and strengthened the translational direction of my work – informing new collaborative projects and approaches to better understand fibrotic mechanisms. It was an inspiring opportunity that reinforced my commitment to advancing understanding of fibrotic lung disease and improving patient outcomes.
Tell us a bit about yourself and how you got interested in pulmonary fibrosis research.
I’m a Research Fellow at the University of Tasmania, with a background in pharmaceutical science and anatomical pathology. My research focuses on understanding the cellular and molecular mechanisms driving lung fibrosis.
I first became interested in pulmonary fibrosis while studying chronic obstructive pulmonary disease, where I observed overlapping inflammatory and fibrotic processes in diseased lungs, especially the small airways and parenchymal destruction. That led me to investigate how epithelial and endothelial cell plasticity contribute to airway and vascular remodelling in IPF.
My work integrates pathology, molecular biology, and translational models, aiming to link tissue-level changes with clinical outcomes. I’m particularly motivated by the unmet clinical need in IPF and the potential to identify novel therapeutic targets.
Alongside research, I teach pathology and laboratory medicine, using examples from fibrosis research to help students connect cellular pathology to real-world patient care — which I find both scientifically and personally fulfilling.
How would you explain your pulmonary fibrosis research to someone unfamiliar with the field?
My research on pulmonary fibrosis aims to understand why lung tissue becomes scarred, how to slow or stop that process, and how to help people breathe better, particularly in IPF. My recent work reported novel findings of fat  tissue deposition in the lungs of patients with IPF. We found that fat  tissue was deposited more in IPF patients than in normal controls, and this was not due to body mass index (BMI), which was not statistically different. This means BMI is not the only factor contributing to lung fat deposits, other factors may also be at play. Further, the mass of fat  tissue and the number of adipocytes negatively correlated with lung function. This suggests that fat tissue is making the intra-parenchymal areas thick, affecting lung function, which could be through a direct effect or by promoting inflammation and fibrosis.
This is one example of what my research is about. I am also focused on other aspects of the pathogenesis in IPF, such as the epithelial and endothelial to mesenchymal transition (EMT/EndMT), which play a key role in small airway and vascular remodelling in IPF patients; the analysis of inflammatory cell population in IPF; and identifying the receptors that respond to infections, and so on. Unless we understand the mechanisms underlying the disease, we cannot design new molecules or identify new biomarkers as therapeutic targets to stop, or even reverse, disease progression. In short, my pulmonary fibrosis research is like detective work—solving the mystery of why lungs scar, how to stop it, and how to help people breathe easier.
Why is this work important?
IPF is a devastating disease with limited treatment options and a median survival of only a few years. To change this, we must first understand why the lungs scar and what drives the progression of tissue damage. My research addresses these fundamental questions.
By identifying adipose tissue deposition in the lungs of IPF patients, independent of BMI, my work reveals a previously unrecognised disease mechanism. Because the amount of adipose tissue correlates with worse lung function, this finding suggests that fat infiltration may directly contribute to tissue thickening, inflammation, and fibrosis. This opens completely new avenues for therapeutic targeting that have not been considered before.
In parallel, my research on EMT/EndMT, airway and vascular remodelling, inflammatory cell populations, and receptors involved in infection responses builds a more complete picture of how IPF develops and progresses. Each piece of evidence helps identify which pathways are driving damage—and which could be blocked or reversed.
Ultimately, this work is important because understanding the mechanisms of fibrosis is the only path to developing new treatments, new biomarkers, and new hope for patients. By uncovering how scarring begins and spreads, my research brings us closer to slowing, stopping, or even reversing this life-limiting disease.
What are the best bits about working in this area?
The best parts of working in pulmonary fibrosis research include making a real difference in patients’ lives, exploring complex and cutting-edge science, and being part of a passionate, collaborative community.
Researchers contribute to transforming lives and offering hope through discoveries that lead to better treatments and diagnostics. The field is scientifically fascinating, involving genetics, immunology, and environmental science, and it embraces precision medicine using AI and genomic data. Collaboration is central, with global teamwork and patient involvement driving progress. Innovation thrives through advanced tools like steam cells and machine learning, and the pace is rapid with new trials and therapies emerging regularly. This work also offers personal growth through continuous learning and strong mentorship. In short, pulmonary fibrosis research is not just about study lungs, it’s about breathing life into science that truly helps people.
What would you like to work on in the future, if funding were not an issue?
If funding were not an issue, I would focus on creating advanced translational models to uncover the metabolic and immune pathways driving pulmonary fibrosis. This would involve integrating multi-omics approaches, such as genomics, proteomics, and metabolomics, with spatial transcriptomics to map cellular interactions in fibrotic lung tissue. I would also invest in high-throughput drug screening platforms to identify novel anti-fibrotic compounds and explore regenerative strategies using stem cells and bioengineered lung scaffolds. Another priority would be building large-scale patient registries and AI-driven predictive tools to personalize treatment and improve early diagnosis. Ultimately, my goal is to bridge basic science and clinical application to accelerate therapies that not only slow fibrosis but reverse it, giving patients a real chance at recovery.