BMC Gastroenterology: Angiogen 2 can predict the degree of hemangiogenic and fibrosis in patients with hepatitis C

Chronic liver damage is known to cause liver fibrosis and eventually cirrhosis and hepatocellular carcinoma (HCC).
pathological angiogenesia and endothial dysfunction are the main drivers of tumor diffusion in the liver.
is considered to be the key pathophysiological mechanism of liver fibrosis.
Sorafini is a molecularly targeted drug for HCC that inhibits angiogenesphage by the subject of endothoste growth factors (VEGF) or plate-derived growth factors, as well as by inhibiting the proliferation of tumor cells through Raf-mediated pathogens and the subject tyrosine kinase.
reported that elevated levels of angiogenesin (ANGP)-2 in the blood of patients with chronic hepatitis C (CHC) were associated with fibrosis.
In this study, the researchers aimed to clarify whether blood ANGP-2 could act as a biomarker for liver angiogenesty and fibrosis in CHC patients, and to further reveal the relationship between this pathology in liver fibrosis mouse models treated with carbon tetrachloride (CCl 4).
results showed elevated plasma ANGP-2 levels in CHC patients compared to healthy volunteers, while the eradication of hepatitis C through direct-acting antiviral drugs reduced ANGP-2 plasma levels.
, plasma ANGP-2 levels were associated with CD31 expression, collagen deposition, clinical fibrosis markers and liver function.
Sorapinib inhibited liver angiogenesty and fibrosis in CCl 4 treated mice and was associated with a decrease in ANGP-2 expression in LSEC.
, the researchers concluded that ANGP-2 could be used as a useful biomarker for liver angiogenesic and fibrosis in CHC patients.
, angiogenesy and fibrosis may be closely related.