The collagen matrix regulates the survival and function of pancreatic islets.

The extracellular matrix (ECM) provides an appropriate microenvironment for many kinds of cells, including pancreatic cells. Collagens are the most abundant components of the ECM. Type I, IV, V and VI collagen has been detected in pancreatic islets, and each type plays important role in the proliferation, survival, function and differentiation of pancreatic cells. In some cases, collagens show behaviours similar to those of growth factors and regulate the biological behaviour of β cells by binding with certain growth factors, including IGFs, EGFs and FGFs. The transcriptional coactivator YAP/TAZ has been widely recognised as a mechanosensor that senses changes in the physical characteristics of the ECM and inhibition of YAP/TAZ enhances insulin production and secretion. Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterised by the destruction of insulin-producing β cells. The crosstalk between collagens and immune cells plays a key role in the development and differentiation of immune cells. Further, Supplementation with collagens during islet transplantation is a promising strategy for improving the quality of the islets. But, excessive collagen deposition results in pancreatic fibrosis and pancreatic carcinoma. Targeting inhibit Piezo, autophagy or IL-6 may reduce excessive collagen deposition-induced pancreatic fibrosis and pancreatic carcinoma. This review provides insights into the treatment of T1DM to prolong life expectancy and provides the potential targets for treating collagen deposition-induced pancreatic fibrosis and pancreatic carcinoma.