PGE2 in fibrosis and cancer: Insights into fibroblast activation

Fibroblasts are the essential cellular architects of connective tissue and as such are crucial cells in contributing to organ homeostasis. While fulfilling important repair functions during tissue regeneration upon wounding, chronic fibroblast activation provokes pathological organ fibrosis and promotes neoplastic disease progression. Identifying targets that may serve to therapeutically terminate fibroblast activation is therefore desirable. Among the mediators that may be relevant in this context is the prostanoid prostaglandin E-2 (PGE(2)) that is produced during inflammatory settings, where pathological fibrosis occurs. Here, we summarize current, in part controversial, concepts on the impact of PGE(2) on fibroblast activation in fibrotic diseases including cancer, and discuss these findings in the context of the evolving concept of fibroblast heterogeneity.