@Article{biocell.2026.085405,
AUTHOR = {Carlo Acierno, Flavia Carriero, Alfredo Caturano, Valentina Rubino, Ferdinando Carlo Sasso, Salvatore D’Angelo, Luca Rinaldi, Giuseppe Terrazzano},
TITLE = {Hepatic Immunometabolic Reprogramming during Systemic Infections: Cellular Pathways Linking Innate Immunity and Metabolic Stress},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27807},
ISSN = {1667-5746},
ABSTRACT = {Systemic infections expose the liver to convergent microbial, inflammatory, vascular, and metabolic stress signals. This narrative review synthesizes how hepatic immunometabolic reprogramming links innate immune sensing, bioenergetic stress, and sepsis-associated liver injury or dysfunction. It focuses on hepatocytes, Kupffer cells, liver sinusoidal endothelial cells, and hepatic stellate cells as a coordinated sinusoidal network rather than isolated cell compartments. Infection-derived pathogen-associated molecular patterns, host-derived damage-associated molecular patterns, cytokines, hypoxia, altered substrate flux, mitochondrial injury, endoplasmic reticulum stress, lipid remodeling, and redox imbalance are integrated into a temporal framework. Early responses may support host defense through acute-phase biosynthesis, microbial clearance, iron restriction, metabolic redistribution, and microvascular coordination. Persistent or spatially disorganized signaling may instead amplify nuclear factor kappa B and inflammasome activation, disrupt adenosine monophosphate-activated protein kinase-mechanistic target of rapamycin-hypoxia-inducible factor 1 alpha balance, impair sinusoidal perfusion, and promote cholestatic, hepatocellular, endothelial, and stromal maladaptation. Pre-existing metabolic dysfunction-associated steatotic liver disease, insulin resistance, aging, sex-related modifiers, and gut-liver axis disruption may lower the threshold for maladaptive trajectories. Evidence-graded biomarkers and clinical phenotypes are therefore framed as hypothesis-generating tools for trajectory-based translational studies.},
DOI = {10.32604/biocell.2026.085405}
}