Fibrosis is defined as the replacement of healthy tissue by an excessive deposition of extracellular matrix, leading gradually to the disturbance and finally to loss of the original tissue architecture and function. Scarring and tissue fibrosis represent major unresolved medical problems resulting in increased morbidity and mortality (1). The initial tissue damage can result from multiple acute or chronic stimuli, including autoimmune reactions, infections, or mechanical injury (s1). Detailed mechanisms how tissue injury leads to tissue fibrosis and how fibrosis can be therapeutically perturbed or reversed are still poorly understood (s2; s3). A thorough investigation of the underlying molecular and cellular components is required to improve therapeutic options for the often devastating pro-fibrotic health conditions. This article is protected by copyright. All rights reserved.