Macrophage MerTK Promotes Liver Fibrosis in Nonalcoholic Steatohepatitis

Bishuang Cai, Paola Dongiovanni, Kathleen E. Corey, Xiaobo Wang, Igor O. Shmarakov, Ze Zheng, Canan Kasikara, Viralkumar Davra, Marica Meroni, Raymond T. Chung, Carla V. Rothlin, Robert F. Schwabe, William S. Blaner, Raymond B. Birge, Luca Valenti, Ira Tabas

Research output: Contribution to journalArticlepeer-review

30 Scopus citations


Genome-wide association studies have indicated that MerTK is a risk factor for liver fibrosis in NASH with an unknown mechanism. Cai et al. discovered that MerTK signaling in liver macrophages, which is enhanced in NASH owing to suppression of its cleavage by ADAM17, promotes TGF-β1 production, HSC activation, and liver fibrosis in NASH.

Original languageAmerican English
Pages (from-to)406-421.e7
JournalCell Metabolism
Issue number2
StatePublished - Feb 4 2020

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


  • ADAM17
  • MerTK
  • MerTK cleavage
  • NASH
  • TGFβ;
  • hepatic stellate cells
  • liver fibrosis
  • macrophage
  • nonalcoholic steatohepatitis
  • retinoic acid


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