Cancer-associated and non-neoplastic fibrosis: Comparative mechanisms and emerging antifibrotic strategies - PubMed
4 hours ago
- #fibrosis
- #antifibrotic strategies
- #cancer-associated fibroblasts
- Fibrosis is a maladaptive tissue-remodeling process involving persistent fibroblast activation, excessive extracellular matrix (ECM) deposition, and tissue stiffening.
- It occurs in both non-neoplastic disorders (e.g., idiopathic pulmonary fibrosis) and solid tumors (e.g., pancreatic, liver, colorectal, and breast cancers), where it contributes to immune evasion, poor drug delivery, and therapeutic resistance.
- Shared mechanisms include TGF-β signaling, ECM remodeling, mechanotransduction, and fibroblast-to-myofibroblast activation, with cancer-associated fibroblast subsets playing a key role in tumor progression and immune modulation.
- Current antifibrotic strategies target ECM components, fibroblast activation, stromal signaling, and tumor-stroma interactions, but face translational limitations.
- Emerging approaches include mesenchymal stromal cell-based platforms and drug repurposing, highlighting opportunities for cross-disciplinary therapies between oncology and fibrotic diseases.
- Comparative analysis of cancerous and non-cancerous fibrosis may reveal shared therapeutic vulnerabilities and support context-specific interventions.