TY - JOUR
T1 - Angiocrine signaling in sinusoidal homeostasis and liver diseases
AU - Gao, Jinhang
AU - Lan, Tian
AU - Kostallari, Enis
AU - Guo, Yangkun
AU - Lai, Enjiang
AU - Guillot, Adrien
AU - Ding, Bisen
AU - Tacke, Frank
AU - Tang, Chengwei
AU - Shah, Vijay H.
N1 - Publisher Copyright:
© 2024 European Association for the Study of the Liver
PY - 2024/9
Y1 - 2024/9
N2 - The hepatic sinusoids are composed of liver sinusoidal endothelial cells (LSECs), which are surrounded by hepatic stellate cells (HSCs) and contain liver-resident macrophages called Kupffer cells, and other patrolling immune cells. All these cells communicate with each other and with hepatocytes to maintain sinusoidal homeostasis and a spectrum of hepatic functions under healthy conditions. Sinusoidal homeostasis is disrupted by metabolites, toxins, viruses, and other pathological factors, leading to liver injury, chronic liver diseases, and cirrhosis. Alterations in hepatic sinusoids are linked to fibrosis progression and portal hypertension. LSECs are crucial regulators of cellular crosstalk within their microenvironment via angiocrine signaling. This review discusses the mechanisms by which angiocrine signaling orchestrates sinusoidal homeostasis, as well as the development of liver diseases. Here, we summarise the crosstalk between LSECs, HSCs, hepatocytes, cholangiocytes, and immune cells in health and disease and comment on potential novel therapeutic methods for treating liver diseases.
AB - The hepatic sinusoids are composed of liver sinusoidal endothelial cells (LSECs), which are surrounded by hepatic stellate cells (HSCs) and contain liver-resident macrophages called Kupffer cells, and other patrolling immune cells. All these cells communicate with each other and with hepatocytes to maintain sinusoidal homeostasis and a spectrum of hepatic functions under healthy conditions. Sinusoidal homeostasis is disrupted by metabolites, toxins, viruses, and other pathological factors, leading to liver injury, chronic liver diseases, and cirrhosis. Alterations in hepatic sinusoids are linked to fibrosis progression and portal hypertension. LSECs are crucial regulators of cellular crosstalk within their microenvironment via angiocrine signaling. This review discusses the mechanisms by which angiocrine signaling orchestrates sinusoidal homeostasis, as well as the development of liver diseases. Here, we summarise the crosstalk between LSECs, HSCs, hepatocytes, cholangiocytes, and immune cells in health and disease and comment on potential novel therapeutic methods for treating liver diseases.
KW - Kupffer cells
KW - MASH
KW - MASLD
KW - NAFLD
KW - NASH
KW - alcoholic liver disease
KW - hepatic stellate cells
KW - liver fibrosis
KW - liver regeneration
KW - liver sinusoidal endothelial cells
KW - metabolic dysfunction-associated steatotic liver disease
KW - portal hypertension
KW - sinusoidal capillarization
UR - http://www.scopus.com/inward/record.url?scp=85196393901&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85196393901&partnerID=8YFLogxK
U2 - 10.1016/j.jhep.2024.05.014
DO - 10.1016/j.jhep.2024.05.014
M3 - Review article
C2 - 38763358
AN - SCOPUS:85196393901
SN - 0168-8278
VL - 81
SP - 543
EP - 561
JO - Journal of hepatology
JF - Journal of hepatology
IS - 3
ER -