This program supports basic, translational, observational, and clinical studies on scleroderma, fibrosis, and autoinflammatory diseases.
Scleroderma is an autoimmune rheumatic disease without an available curative therapy. It is a heterogenous and complex disease that can be categorized as localized scleroderma (morphea) and systemic scleroderma. While etiology of scleroderma is poorly understood, abnormal vasculature, inflammation, and fibrosis are main characteristics of the disease with diverse clinical manifestations (e.g. Raynaud’s phenomenon, digital ulcers, fibrosis in skin and internal organs). Fibrosis is an exaggerated wound healing process which is characterized by a progressive scarring and hardening of tissues with excessive deposition of extracellular matrix. This program supports research on scleroderma, fibrotic diseases, and fibrotic comorbidities associated with rheumatic diseases (e.g. Interstitial lung disease).
Another axis of this program lies on research on the autoinflammatory and inflammasome-mediated diseases characterized by defect(s) or dysregulation on the predominantly innate immune system or inflammasome activity (e.g. gout, juvenile idiopathic arthritis, spondyloarthropathies).
Within each of these portfolio areas, studies could emphasize, but are not limited to, any of the following:
- Molecular and cellular mechanisms of pathogenesis and pathophysiology
- Identification of unique genomic, epigenomic, and proteomic signatures
- Immune cells or non-immune cells (e.g. fibroblasts, endothelium, pericytes, and adipocytes) or cross-talk among different cell types leading to impaired inflammation resolution, acute and chronic inflammation, and fibrosis
- Development of animal and organoid models
- Translational and observational and clinical research (e.g. development of diagnosis and therapy, establishment of patient registry and biorepository)