IL6ST (gp130) binding proteins, such as HyperIL6, promote liver regrowth in a STAT3-indpependent manner through competitive inhibition of anti-regenerative IL11 signaling.

Genetic mouse models show that hepatic NIK and IKKα inhibit hepatocyte proliferation and liver regeneration in part by inhibiting the JAK2/STAT3 pathway.

Lutheran is a novel marker for classification of bile duct remodeling in distinct liver injury, and an interesting functional molecule for investigating the nature of liver stem/progenitor cells during regeneration.

Mammalian cellular iron homeostasis and the maturation of the cytosolic iron sulfur cluster proteins are dependent on the mitochondrial protein import machinery.

Mouse genetic studies reveal that let-7 performs potent tumor suppressive roles, but at the expense of regeneration and tissue homeostasis in the liver, findings with unanticipated therapeutic implications.

A new type of mRNAs-loaded CD133⁺ vesicles, named intercellsome, mediate cell-cell communications to compensate intracellular proliferative signal deficit, representing a previously unrecognized mechanism of cell proliferation under stress.

Chronic fat overload triggers the conversion of quiescent biliary epithelial cells into proliferative progenitors through an E2F-dependent mechanism.

HepG2 transmitochondrial cybrids of haplogroup J genome had increased sensitivity to aspects of mitochondrial dysfunction induced by tolcapone and 2-hydroxyflutamide, compared to haplogroup H, thus cybrids provide a practical system to investigate the consequences of mitochondrial genome on drug-induced hepatotoxicity.

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%.

Mecp2 expression is cell cycle-dependent and negatively regulates quiescence exit.