Fibrosis is the final stage of the development of chronic
inflammation. It is characterized by excessive deposition of the extracellular matrix, leading to tissue structure damage and organ dysfunction, which is a serious threat to human health and life. However, the molecular mechanism of
fibrosis is still unclear.
Inflammasome is a molecular complex of
proteins that has been becoming a key innate sensor for host immunity and is involved in pyroptosis, pathogen
infection,
metabolic syndrome, cellular stress, and
tumor metastasis.
Inflammasome signaling and downstream
cytokine responses mediated by the
inflammasome have been found to play an important role in
fibrosis. The
inflammasome regulates the secretion of IL-1β and
IL-18, which are both critical for the process of
fibrosis. Recently, researches on the function of
inflammasome have attracted extensive attention, and data derived from these researches have increased our understanding of the effects and regulation of
inflammasome during
fibrosis. In this review, we emphasize the growing evidence for both indirect and direct effects of
inflammasomes in triggering
fibrosis as well as potential novel targets for antifibrotic
therapies.