UW-Madison researchers get nearly $11M to study what drives IPF
Interdisciplinary team will study cellular processes that promote lung scarring
An interdisciplinary group of researchers at the University of Wisconsin (UW)-Madison have received nearly $11 million to study the biological processes that promote lung scarring in idiopathic pulmonary fibrosis (IPF).
Funding comes from a four-year grant (HT94252410543) provided by the U.S. Department of Defense.
The research will be spearheaded by Allan Brasier, MD, executive director of the Institute for Clinical and Translational Research at UW-Madison, who is a leading global researcher on the role of inflammation in heart and lung diseases. Brasier will work with collaborators across a range of disciplines to get the work done.
“An interdisciplinary approach where cell biologists, engineers, lung doctors and medicinal chemists are all able to work closely together is key to tackling a difficult disease like IPF,” Brasier said in a university news story. “This program provides a template for pushing the envelope to address otherwise intractable research problems through harnessing the clinical and research strengths here at UW-Madison.”
IPF is a disease characterized by progressive lung scarring (fibrosis) and inflammation that make it increasingly harder to breathe. There is no cure for the condition, and once the lungs become too damaged to function properly, a lung transplant may be a patient’s best option. Patients live an average of three to five years after a diagnosis.
Few treatments are approved to slow IPF progression
Despite these serious consequences, few approved treatments are available for slowing IPF progression and prolonging patient survival.
The lack of effective therapies could in part be because the exact cause of the chronic lung disease and the molecular factors that drive its progression are unclear.
With the recent four-year funding, Brasier and colleagues will embark on a research project, titled “Cell-matrix Interactions Promoting Idiopathic Pulmonary Fibrosis,” to better understand the mechanisms underlying IPF.
Cell-matrix interactions refer to interactions between cells and their surrounding matrix, or extracellular matrix (ECM), which provides structural support to cells and tissues. The ECM also influences the growth, maturation, and movement of cells, as well as tissue repair.
In IPF, excessive production of ECM components contributes to lung scarring, and cell-matrix interactions have been suggested to play a key role in the maturation or reversion of myofibroblasts, the main cell type implicated in pulmonary fibrosis.
Team will use AI and advanced 3D modeling
Specifically, the team will investigate the cellular processes that drive atypical lung cell responses known to contribute to disease progression. The team will use artificial intelligence and advanced three-dimensional modeling to aid their research.
The scientists will also work on refining new imaging techniques for measuring cellular metabolism and developing targeted drug delivery systems to maximize the benefits of therapies for the lung disease.
“New, creative and transdisciplinary research teams are needed to push the boundaries of existing disciplines to address this complex disease,” Brasier said.
The researchers have been working over the last three years to launch the collaboration.
“This program is a superb example of bringing UW-Madison’s strengths in transdisciplinary research to address a major unmet health need,” said Cynthia Czajkowski, PhD, interim vice chancellor for research at UW-Madison. “The research strengths from across campus will advance mechanistic understanding and diagnostics for IPF.”
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