Zhao Shan

The paper identifies a stress-response program in mid-zone hepatocytes during early acute liver injury that suppresses proliferation via the Atf4-Chop-Btg2 axis.

This study shows platelets worsen acute liver injury by transferring aldolase A via extracellular vesicles to Kupffer cells, promoting inflammation and injury.

This study identifies bacterial peptidoglycan as a conserved activator of lysosomal function that extends lifespan in C. elegans and mice by enhancing V-ATPase activity and lysosomal acidification.

This study identifies hyperactivated glycolysis as a driver of spatially-patterned Kupffer cell depletion in MASLD, suggesting glucose metabolism as a therapeutic target.

This study identifies how bacterial tryptophan metabolism activates lysosomal function to promote lipid breakdown and reduce hepatic steatosis in both C. elegans and mice.

This study identifies microbial peptidoglycan as a mitophagy inducer that protects against hepatocyte death and liver fibrosis by interacting with p62.

This study identifies Chi3l1 as a metabolic regulator that differentially affects hepatic macrophage fate in MASLD by modulating glucose metabolism in Kupffer cells.

The paper identifies a bacterial sensing mechanism in neurons that activates intestinal mitochondrial surveillance to protect against infections.

This study shows that neurons detect harmful food sources and trigger systemic digestive shutdown to avoid harm.