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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 journal › Article › peer-review

Abstract

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 languageEnglish (US)
Pages (from-to)406-421.e7
JournalCell Metabolism
Volume31
Issue number2
DOIs
StatePublished - Feb 4 2020
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2019 Elsevier Inc.

Keywords

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

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