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Fibrotic diseases is a cover term coined by our laboratory to address complications of the excessive scarring of fibrous tissue. They occur when fibroblasts – a critical component of the structural tissue of the body – proliferate and include, but are not limited to lung fibrosis, kidney and liver fibrosis, scleroderma, bone marrow fibrosis, wound healing and surgical adhesions. Despite fibrotic diseases being life-threatening-- the mortality rate of some are higher than that of cancer-- current treatments are ineffective and/or entirely nonexistent. Our mission is to identify new targets for treatment through uncovering the underlying mechanisms of inflammation and fibrosis. We seek to understand how fibroblasts crosstalk with one another, with the immune system, and with epithelial and mesenchymal cells. By integrating single-cell transcriptional profiling, next-generation shotgun proteomics with mass cytometry and chromatin studies of patient-derived primary tissues in combination with in vivo modeling of fibrotic disease in mice, we gain insight into the pathophysiology of fibrotic diseases. We employ immunotherapy combined with small molecules in order to manipulate signaling pathways at the transcriptional level to disrupt pro-fibrotic cell function and fate. The transcriptional networks we study play key roles in fibrotic disease, metabolism, bone physiology, cancer, and immunology. Understanding them will provide the critical foundation to translate our findings into immunotherapies and clinical practice for fibrotic diseases.