fibrosis

Definition

Fibrosis is a pathological wound-healing response characterized by excessive accumulation of extracellular matrix (ECM) components, particularly collagen, leading to tissue scarring and organ dysfunction. It occurs when chronic inflammation or repeated tissue injury triggers persistent activation of fibroblasts and myofibroblasts, which overproduce ECM proteins. Fibrosis affects multiple organs including liver (cirrhosis), lungs (pulmonary fibrosis), heart (cardiac fibrosis), and kidneys (renal fibrosis). Key molecular drivers include transforming growth factor-beta (TGF-β) signaling, inflammatory cytokines, and dysregulated ECM remodeling. Understanding fibrotic mechanisms is critical for developing therapeutic interventions, as fibrosis contributes to approximately 45% of deaths in developed countries and currently has limited treatment options.

Visualize fibrosis in Nodes Bio

Researchers can map fibrotic signaling cascades by visualizing TGF-β pathway interactions, ECM protein networks, and inflammatory mediator relationships. Network analysis reveals central regulatory nodes like SMAD proteins, matrix metalloproteinases, and profibrotic cytokines. Users can integrate multi-omics data to identify dysregulated pathways across different fibrotic conditions, compare organ-specific fibrotic signatures, and discover potential therapeutic targets through network-based drug repurposing approaches.

Example Use Case

A pharmaceutical team investigating idiopathic pulmonary fibrosis (IPF) uses network analysis to map interactions between 150 differentially expressed genes from patient lung biopsies. They identify a highly connected subnetwork centered on TGF-β1, CTGF, and COL1A1, revealing unexpected crosstalk between Wnt/β-catenin and TGF-β pathways. By overlaying drug-target data, they discover that a repurposed kinase inhibitor targeting three hub proteins shows promise for disrupting the fibrotic cascade, leading to preclinical validation studies.