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JAM-A is a multifaceted regulator in hepatic fibrogenesis, supporting LSEC integrity and stellate cell quiescence.

Jonathan Frederik BrozatElisa F BrandtMyriam StarkPetra FischerTheresa H WirtzAlexander FlaßhoveAaron N RodenhausenTanja VajenAlexandra C A HeinzmannSophia M-T SchmitzSamira Abu JhaishaAnjali A RöthRory R KoenenHacer SahinChristian TrautweinMarie-Luise Berres
Published in: Liver international : official journal of the International Association for the Study of the Liver (2022)
Our models decipher cell-specific JAM-A to exert crucial functions during hepatic fibrogenesis. JAM-A on bone marrow-derived cells regulates non-sinusoidal vascular immune cell recruitment, while endothelial JAM-A controls liver sinusoid capillarization and HSC quiescence.
Keyphrases
  • single cell
  • cell therapy
  • induced apoptosis
  • endothelial cells
  • stem cells
  • cell cycle arrest
  • bone marrow
  • endoplasmic reticulum stress