Complement C1q mediates the expansion of periportal hepatic progenitor cells in senescence-associated inflammatory liver.

This study has identified C1q in the chronic hepatitis liver as an unorthodox signal for activating the essential β-catenin pathway in hepatic progenitor cells (HPCs) and liver tumors, which is critical for their proliferation and dedifferentiation. Inhibition of C1q not only effectively suppressed the expansion, but also facilitated the differentiation of HPCs and liver tumors. However, it spared the orthodox β-catenin function in pericentral normal hepatocytes. C1q thus becomes a potential therapeutic target for liver tumors derived from HPCs in patients with chronic hepatitis.