After injury, organs repair in an attempt to restore normal tissue architecture and function. Such repair involves a complex interplay between progenitor cells, inflammatory cells, cytokines and the extracellular matrix resulting in tissue regeneration and matrix remodeling. Chronic injury results in the common end-point of organ fibrosis which is a combination of inadequate numbers of functioning cells and a scarred fibrotic matrix.
Organ fibrosis results in a great deal of morbidity and mortality due to diseases such as idiopathic pulmonary fibrosis, liver cirrhosis, renal fibrosis, and myelofibrosis. The demographic changes of an aging population and the obesity epidemic are further increasing the number of patients affected by fibrosis, and have raised its profile among patients, clinicians and industry. This increasing clinical need has been paralleled by a greater understanding of the basic biology of tissue regeneration and fibrosis, and a realization that many of the key pathways involved in both processes are shared between organs, leading to a shift away from viewing fibrosis as a distinct tissue-specific disease process towards that of a failure of regeneration and matrix remodeling that is common to many organs.