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%.

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.

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

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

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.

The liver-specific miRNA microRNA-122 plays a previously unknown role in hepatocyte intrinsic innate immunity by targeting the RTKs/STAT3 signaling pathway.

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

Chromosomal instability through spindle assembly checkpoint alleviation facilitates malignant transformation of hepatocytes and T-cells in vivo, resulting in cancers with recurrent karyotypes.

Host CD81 and Scavenger Receptor BI operate independently to mediate invasion of hepatocytes by different species of Plasmodium sporozoites, which use the parasite protein P36 as a key determinant of the entry route.

The combination of in vitro investigations, the zebrafish screening model and rodent experiments offered a unique approach to optimizing nanoparticles modified with Hepatitis B virus-derived peptides to specifically target hepatocytes.