A comparative analysis of the molecular basis of fibrosis between tissues

The aim of effective healing is to restore comparable structure and function to tissues. In some circumstances, this is not achieved, resulting in fibrotic scar tissue formation. Although this may have offered survival advantages in the past, fibrosis leads to functional disruption, organ failure and even death. Fibrosis affects many tissues types, but its ramifications are arguably most conspicuous in the skin. Dermal fibrosis impacts millions of people worldwide, and currently, treatment is not directed against a given molecular abnormality. Research demonstrates a complex picture of cellular and molecular interaction culminating in the deposition of fibrotic tissue. This article discusses key molecular mechanisms of fibrosis within tissues and highlights the similarities and differences amongst key pathways. There is compelling evidence for the involvement of toll-like receptor-4 and transforming growth factor β within fibrosis throughout all tissue types. With regards to other molecules, although there are similarities between tissues, evidence is inconsistent. In order to gain therapeutic advances in the prevention or treatment of fibrosis, research should strive to understand specific molecular mechanisms in models that closely replicate human disease. Further, there should be a healthy scepticism regarding the applicability of given molecular targets between settings. This review highlights a number of prime movers to fibrosis that are the focus of current research.