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Updated: Jan 24, 2026

Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin
Published on: September 12, 2019
PGE2 in fibrosis and cancer: Insights into fibroblast activation
Eiman Elwakeel1, Bernhard Brüne2, Andreas Weigert1
1Institute of Biochemistry I, Faculty of Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.
Abstract:
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 E2 (PGE2) that is produced during inflammatory settings, where pathological fibrosis occurs. Here, we summarize current, in part controversial, concepts on the impact of PGE2 on fibroblast activation in fibrotic diseases including cancer, and discuss these findings in the context of the evolving concept of fibroblast heterogeneity.
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