ReviewHepatology communications2026
Hepatocyte senescence in metabolic dysfunction-associated steatotic liver disease (MASLD).
Review in Hepatology communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Authors and funding
8 authors.
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Abstract
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major global health challenge, with particularly high morbidity and disease burden. Cellular senescence has been identified as one of the core mechanisms driving the onset and progression of MASLD. Hepatocytes, the primary functional cells of the liver, can undergo a senescent state under metabolic stress. These senescent hepatocytes secrete a series of pro-inflammatory and profibrotic factors, directly exacerbating hepatic inflammation and activating hepatic stellate cells, thereby leading to pathological fibrosis. The purpose of this review is to explore the key molecular pathways of hepatocyte senescence and their impact on MASLD progression. Finally, we discuss relevant intervention strategies that can be used for the prevention and treatment of MASLD.
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