Figure 1

Highlights of the pathophysiology of fibrosis. Injury will lead to both activation of the immune system as well as activation of pericytes and fibroblasts. Pericytes and fibroblasts can differentiate into myofibroblassts and many factors, listed here next to the arrow, have an influence on this process. Myofibroblasts contribute to the secretion and remodeling of extracellular matrix, thereby inducing fibrosis. miR29a can inhibit fibrosis. Inflammation also has a role in injury and subsequent fibrosis. Attracted leukocytes clear up debris and secrete inflammatory molecules. A lot of factors can influence the inflammatory response, such as NOX-1/4 which is known to be involved in the influx of macrophages. When the damage is repaired and a fibrotic scar is formed, myofibroblasts can either go into apoptosis or become quiescent fibroblasts. Biomarkers for this fibrotic mechanism are listed in purple. Furthermore, there are current preclinical and clinical trials trying to inhibit fibrosis. The molecules and drugs from these trials are shown in grey.