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Войти в исследования Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · 2026
Circulating hepatocyte-derived extracellular particles as potential biomarker of steatohepatitis progression to fibrogenesis: Exploring the impact of smoking.
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Masrour Oumnia, Morvan Justine, Rapin Alison, Aimé Alexis, Burel Agnès, Genêt Valentine, Brisset Stéphanie, Lagadic-Gossmann Dominique, Bardou-Jacquet Edouard, Martin-Chouly Corinne
Аннотация
BACKGROUND: Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) encompasses a spectrum of liver conditions, primarily driven by metabolic factors and characterized by steatosis. Extracellular vesicles and particles (EVPs) are emerging as biomarkers for liver diseases as they reflect the state of their cells of origin and carry molecular cargo that can influence disease progression. We aimed to explore the role of EVPs with MASLD progression, smoking impact and EVPs effect on macrophages.
METHODS: We analyzed EVPs using nanoparticle tracking analysis, transmission electron microscopy and flow cytometry. Cytokine expressions were quantified in EVPs-exposed macrophages.
RESULTS: We showed that EVP number is higher in patients with steatohepatitis and they were correlated with the severity of liver inflammation and steatosis, as well as with biological markers. In particular CD63+-ASGR1+-EVPs were notably more prevalent in blood of patients with steatohepatitis. Active smoking further increased EVP numbers and CD63+-ASGR1+-EVPs in MASLD patients. Functionally, exposure of macrophages to CD63+-EVPs from MASLD patients induced TGF-β and TIMP-1 secretion.
CONCLUSION: This study highlights the potential of EVs as biomarkers for MASLD progression and their role in mediating disease mechanisms via intercellular communication, notably by their potential to contribute to fibrogenic signaling. Although exploratory, the study also highlights the potential impact of the exposome, particularly smoking, on MASLD pathogenesis.
METHODS: We analyzed EVPs using nanoparticle tracking analysis, transmission electron microscopy and flow cytometry. Cytokine expressions were quantified in EVPs-exposed macrophages.
RESULTS: We showed that EVP number is higher in patients with steatohepatitis and they were correlated with the severity of liver inflammation and steatosis, as well as with biological markers. In particular CD63+-ASGR1+-EVPs were notably more prevalent in blood of patients with steatohepatitis. Active smoking further increased EVP numbers and CD63+-ASGR1+-EVPs in MASLD patients. Functionally, exposure of macrophages to CD63+-EVPs from MASLD patients induced TGF-β and TIMP-1 secretion.
CONCLUSION: This study highlights the potential of EVs as biomarkers for MASLD progression and their role in mediating disease mechanisms via intercellular communication, notably by their potential to contribute to fibrogenic signaling. Although exploratory, the study also highlights the potential impact of the exposome, particularly smoking, on MASLD pathogenesis.