Abstract
Fibrosis, a maladaptive response characterized by excessive extracellular matrix deposition, disrupts tissue architecture and organ function. Recent advances reveal fibroblast heterogeneity across organs, with shared Postn(+) activated fibroblast subsets driving fibrogenesis. Emerging evidence links fibrosis to mechanical stress, metabolic rewiring, and non-coding RNA regulation, unveiling novel therapeutic targets. Innovative models and regenerative strategies - including senolytics, metabolic modulation, and in vivo reprogramming – hold promise to reverse fibrosis and promote tissue repair.