In a new article just now out in Nature Biomedical Engineering, Professor Andrew Emili and colleagues report signaling perturbations in fibrotic heart tissue from human patients and transgenic mice suffering from hypertrophic cardiomyopathy, and in an organ-on-a-chip (OOC) model of cardiovascular disease. Using quantitative phosphoproteomic profiling and integrative analyses, they identified pathway-level changes associated with maladaptive pro-fibrotic responses in diseased cardiac tissue. Given that preventing or reversing fibrosis is indicated for clinical management of heart failure and improving clinical outcomes, this study provides mechanistic insights and potential therapeutic avenues, while laying the groundwork for a follow up collaborative project with Chris Chen’s team at the BU BioDesign Center supported by the Kilachand Multicellular Design Program.