Forward programming of human pluripotent stem cells with a combination of four transcription factors allows the production of functional hepatocytes.

Human chemically induced liver progenitors (hCLiPs), which are generated from primary human hepatocytes, exhibit the potential to repopulate injured livers of host mice with efficiency > 90%.

Hepatocytes proliferate to maintain a constant liver-to-body mass ratio during intermittent fasting.

Loss of hepatic Cdk1 leads to oxidative stress, increased fatty acids in blood, and hyperinsulinemia, which resulted in insulin resistance and hepatic steatosis, similar as in diabetes.

NOD-like receptor NLRP12 is a critical regulator of hepatocyte proliferation and its activation could be therapeutically used to suppress hepatocellular carcinoma.

A muscle-derived signaling molecule suppresses excessive accumulation of lipids in the Drosophila adipose tissue by activating the Pi3K/Akt/mTOR signaling cascade in the Drosophila hepatocyte-like cells.

Physical and functional interactions between HNF4A and TAF4 coordinate HNF4A genomic occupancy with pre-initiation complex formation to activate post-natal hepatocyte gene expression.

Biochemical and genetic approaches reveal how the focal adhesion protein kindlin-2 controls the liver development and homeostasis by reducing inflammation.

Studies in murine model identify hepatic Rela-Stat3 network as a potential driver of gut inflammation and a novel therapeutic target for inflammatory bowel disease, offering new insights into liver-gut crosstalk.

Store operated calcium entry is defective in hepatocytes of obese mice, and restoring this process is sufficient to improve glucose metabolism.