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Published on: November 10, 2021
Cytokines and renin-angiotensin system signaling in hepatic fibrosis
Montserrat Moreno1, Ramon Bataller
1Liver Unit, Institut Clínic de Malalties Digestives i Metabòliques, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Catalonia, Spain.
Abstract:
Hepatic fibrosis is the result of a complex interplay between resident hepatic cells, infiltrating inflammatory cells, and a number of locally acting peptides called cytokines. Key mediators include transforming growth factor b1, vasoactive substances, adipokines, inflammatory cytokines and chemokines. Angiotensin II, the main effector of the renin-angiotensin system, is a true cytokine that plays a major role in liver fibrosis. Angiotensin II is locally synthesized in the injured liver and induces profibrogenic actions in hepatic stellate cells. Drugs blocking the renin-angiotensin system are promising antifibrotic agents. There are multiple signal transduction pathways involved in cytokine signaling. Drugs interfering intracellular pathways involved in increased collagen production are potential therapies for liver fibrosis.
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