Tracing the origins of fibrotic fibroblasts: does the name matter? Look at the genes!

Organ fibrosis is a major contributor to global mortality, with projections suggesting that by 2030, 45% of deaths will be linked to fibrotic diseases [1]. Fibrosis is essentially a pathological scarring process, characterised by an excessive buildup of extracellular matrix (ECM) components that distorts the structure and function of affected organs. No matter the initial cause of injury or the organ affected, fibrosis develops through the secretion of ECM proteins by pathological myofibroblasts, which can be characterised by the expression of several markers, such as ACTA2, FAP, POSTN or CTHRC1, and by an increased expression of ECM proteins [2].