Wound Healing & Fibrosis

Wound healing progresses via 3 overlapping phases: inflammation, granulation, and tissue remodeling. After cutaneous injury, a blood clot forms, and inflammatory cells infiltrate the wound, secreting cytokines and growth factors to initiate the inflammation phase. During the granulation phase, fibroblasts and other cells differentiate into myofibroblasts, which deposit extracellular matrix (ECM) proteins. Simultaneously, angiogenesis occurs, and keratinocytes proliferate and migrate to close the wound. In the final tissue remodeling phase, apoptosis eliminates myofibroblasts and extraneous blood vessels, and the ECM is remodeled to resemble the original tissue. Fibrosis occurs when inappropriate tissue remodeling results in excess ECM deposition due to myofibroblast survival or lack of ECM proteolytic degradation. At the other extreme of wound healing pathophysiology, chronic wounds feature dysregulated tissue remodeling with enhanced ECM degradation. As wound healing and its dysregulation via fibrosis and other means occur in all tissues, analysis of these mechanisms may yield novel drug targets for a variety of disorders.

QIAGEN provides a broad range of assay technologies for wound healing and fibrosis research that enables analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for wound healing and fibrosis studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.