Macrophages and platelets in liver fibrosis and hepatocellular carcinoma
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Macrophages and platelets in liver fibrosis and hepatocellular carcinoma. / Casari, Martina; Siegl, Dominik; Deppermann, Carsten; Schuppan, Detlef.
In: FRONT IMMUNOL, Vol. 14, 2023, p. 1277808.Research output: SCORING: Contribution to journal › SCORING: Review article › Research
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TY - JOUR
T1 - Macrophages and platelets in liver fibrosis and hepatocellular carcinoma
AU - Casari, Martina
AU - Siegl, Dominik
AU - Deppermann, Carsten
AU - Schuppan, Detlef
N1 - Copyright © 2023 Casari, Siegl, Deppermann and Schuppan.
PY - 2023
Y1 - 2023
N2 - During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased susceptibility to infection. At an early stage, liver fibrosis is a dynamic and reversible process, however, from the cirrhotic stage, there is significant progression to hepatocellular carcinoma. Both liver-resident macrophages (Kupffer cells) and monocyte-derived macrophages are important drivers of fibrosis progression, but can also induce its regression once triggers of chronic inflammation are eliminated. In liver cancer, they are attracted to the tumor site to become tumor-associated macrophages (TAMs) polarized towards a M2- anti-inflammatory/tumor-promoting phenotype. Besides their role in thrombosis and hemostasis, platelets can also stimulate fibrosis and tumor development by secreting profibrogenic factors and regulating the innate immune response, e.g., by interacting with monocytes and macrophages. Here, we review recent literature on the role of macrophages and platelets and their interplay in liver fibrosis and hepatocellular carcinoma.
AB - During fibrosis, (myo)fibroblasts deposit large amounts of extracellular matrix proteins, thereby replacing healthy functional tissue. In liver fibrosis, this leads to the loss of hepatocyte function, portal hypertension, variceal bleeding, and increased susceptibility to infection. At an early stage, liver fibrosis is a dynamic and reversible process, however, from the cirrhotic stage, there is significant progression to hepatocellular carcinoma. Both liver-resident macrophages (Kupffer cells) and monocyte-derived macrophages are important drivers of fibrosis progression, but can also induce its regression once triggers of chronic inflammation are eliminated. In liver cancer, they are attracted to the tumor site to become tumor-associated macrophages (TAMs) polarized towards a M2- anti-inflammatory/tumor-promoting phenotype. Besides their role in thrombosis and hemostasis, platelets can also stimulate fibrosis and tumor development by secreting profibrogenic factors and regulating the innate immune response, e.g., by interacting with monocytes and macrophages. Here, we review recent literature on the role of macrophages and platelets and their interplay in liver fibrosis and hepatocellular carcinoma.
KW - Humans
KW - Carcinoma, Hepatocellular/pathology
KW - Esophageal and Gastric Varices/metabolism
KW - Liver Neoplasms/pathology
KW - Gastrointestinal Hemorrhage
KW - Liver Cirrhosis
KW - Macrophages
KW - Fibrosis
U2 - 10.3389/fimmu.2023.1277808
DO - 10.3389/fimmu.2023.1277808
M3 - SCORING: Review article
C2 - 38116017
VL - 14
SP - 1277808
JO - FRONT IMMUNOL
JF - FRONT IMMUNOL
SN - 1664-3224
ER -