Review summarizes immune interactions and their role in disease progression of steatotic liver disease, suggesting therapeutic targets.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the leading chronic liver disorder worldwide. Its pathological progression typically begins with hepatic steatosis, advances to metabolic dysfunction-associated steatohepatitis (MASH) and fibrosis, and in some cases culminates in hepatocellular carcinoma (HCC). This continuum is influenced not only by metabolic disturbances but also by coordinated local and systemic inflammatory and immune responses. This article systematically summarizes the inflammatory mechanisms underlying MASLD/MASH progression, highlighting their origin in the dynamic crosstalk between innate and adaptive immune compartments. Such interactions involve multiple immune cell subsets, including macrophages, T lymphocytes, and B lymphocytes, and are governed by intricate molecular regulatory pathways. Furthermore, this review explores how these interconnected processes amplify hepatic inflammation and fibrogenesis and discusses potential therapeutic approaches to modulate key nodes within immune signaling networks.
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Li et al. (2026) studied this question.
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