Synapse
⌘+K
Synapse
PulseExploreClubsResearchersJournals
Instagram
HomeClubsExplore
September 16, 2025Journal of Clinical InvestigationOpen Access

MASH: the nexus of metabolism, inflammation, and fibrosis

View Full Paper
Ask AI
Bookmark
Share

Authors

GSGregory R. SteinbergACAndré C. CarpentierDWDongdong Wang

Discussion

Loading...

Member takes

Overview

Review outlines key metabolic factors driving inflammation and fibrosis in MASH, suggesting critical intercellular signaling pathways.

Key Points

  • MASH is characterized by hepatocyte injury and promotes a cycle of inflammation and fibrosis.
  • Key metabolites, including saturated fatty acids and free cholesterol, reinforce inflammatory responses across liver cells.
  • Crosstalk between hepatocytes, macrophages, and hepatic stellate cells escalates liver injury and disrupts metabolism.
  • Understanding MASH pathogenesis highlights the complex interaction of nutrient excess and chronic liver inflammation.

Cite This Study

Steinberg et al. (2025) studied this question.

synapsesocial.com/papers/68d42336713b0b5dfea6b68dhttps://doi.org/10.1172/jci186420
View Full Paper
Ask AI
Bookmark
Share

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Metabolomic, Lipidomic, and Enterohormone Changes in the Progression from MASLD to MASH2025
  2. 2The heterogeneity of monocyte-derived macrophages in MASH pathogenesis2025
  3. 3Gut microbes mediate the synergistic effects of dietary cholesterol and saturated fat in driving fibrosing MASH2025
  4. 4Metabolic and genetic mechanisms of metabolic dysfunction-associated steatotic liver disease: an integrative perspective from molecular pathways to clinical challenges2025 · 18 citations
  5. 5Impaired TIM4-mediated efferocytosis by liver macrophages contributes to fibrosis in metabolic dysfunction–associated steatohepatitis2025