Researchers at the German Cancer Research Center Deutsches Krebsforschungszentrum (DKFZ) and their collaborators have cast new light on the mechanisms by which hepatic stellate cells control liver metabolism and regeneration. The work builds on the concept of angiocrine signaling, established 15 years ago.
Inflammatory bowel disease (IBD) is impacted by genetic, environmental and immunological factors, where the imbalance in T-cell immune responses significantly promotes its progression. In recent years, the role of RNA modifications in epigenetic regulation has caught significant attention in research; among these, N4-acetylcytidine (ac4C) is the only acetylation process in RNA and plays a role in several biological processes, but its implication in the functioning of immune cells is largely unknown to date.
The Ca2+ stored in the cellular endoplasmic reticulum (ER) plays a crucial role in protein folding and lipid transfer, and its impairment leads to cellular ER stress. When chronic cellular ER stress occurs in the liver, it triggers the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH). Previous reports found that NACHT and WD repeat domain containing 1 (NWD1) localized in the ER and mitochondria in neural stem/progenitor cells, but the significance of NWD1 outside the brain is not well known.
