Pro-fibrotic Phenotype of Human Skin Fibroblasts Induced by Periostin via Modulating TGF-β Signaling

Excessive accumulation of extracellular matrix (ECM) components is a hallmark of organ fibrosis. It is a final common outcome for several diseases, including fibroproliferative disorders such as systemic sclerosis (SSc) and idiopathic pulmonary fibrosis (IPF), which leads to significant morbidity and mortality [1]. Unfortunately, no effective therapy for organ fibrosis is yet available. Uncontrolled wound healing responses, including acute and chronic inflammation, angiogenesis, activation of resident cells, and abnormal ECM remodeling, are thought to be involved in the pathogenesis of fibrosis.