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Multi‐scale Computational Model of Endothelial Cell‐Pericyte Coupling in Idiopathic Pulmonary Fibrosis

Microvascular stability is highly dependent on endothelial cell‐pericyte coupling. In fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF), extracellular matrix stiffening and elevated concentrations of profibrotic factors, such as TGF‐β, can disrupt this cell‐cell communication. Treatment of IPF with the antifibrotic drug Nintedanib, which targets PDGF‐βR, FGF‐R, and VEGF‐R signaling, may counteract these effects to strengthen endothelial cell‐pericyte coupling and promote microvessel stability1,2. We have developed a multi‐scale computational model that simulates intracellular signaling in endothelial cells and pericytes, heterotypic cell‐cell communication, and the dynamic lung microenvironment to study how Nintedanib2 and other drugs affect microvascular network remodeling in IPF. We hypothesize that blocking PDGF‐βR and FGF‐R signaling with Nintedanib is sufficient to rescue TGF‐β‐induced endothelial cell‐pericyte decoupling.