Serum vascular cell adhesion molecule-1 predicts significant liver fibrosis in non-alcoholic fatty liver disease

Abstract

VCAM-1 levels are able to accurately predict significant (⩾F2) fibrosis in NAFLD patients.

Omentin‐regulated proteins combine a pro‐inflammatory phenotype with an anti‐inflammatory counterregulation in human adipocytes: A proteomics analysis

“…In our dataset, predominantly VCAM‐1 and ICAM‐1 as well as MMP2 and TIMP1 were upregulated by omentin and involved in this pathway. Serum levels of VCAM‐1 and ICAM‐1 are predictors of hepatic fibrosis and hepatocellular carcinoma risk, respectively . Interestingly, the transcriptional activation of TIMP‐1 and MMP‐2 is important for the pathogenesis of liver fibrosis .…”

“…Serum levels of VCAM-1 and ICAM-1 are predictors of hepatic fibrosis and hepatocellular carcinoma risk, respectively. 54,55 Interestingly, the transcriptional activation of TIMP-1 and MMP-2 is important for the pathogenesis of liver fibrosis. 53 The potential link between these pro- Interestingly, the most activated upstream cytokines IL-1β and TNFα regulate the activity of NFκB, and all three classes of MAPK (JNK, ERK1/2, and p38 MAPK).…”

Angiopoietin‐2 Promotes Pathological Angiogenesis and Is a Therapeutic Target in Murine Nonalcoholic Fatty Liver Disease

“…Our group previously demonstrated that blocking VEGF receptor 2 reduces hepatic angiogenesis and attenuates hepatic steatosis and inflammation in a NASH mouse model . In addition, we have recently reported elevated vascular cell adhesion molecule 1 (VCAM‐1) serum levels in NAFLD patients, which might have clinical utility as a biomarker for the diagnosis of significant fibrosis . However, although VEGF and multiple tyrosine kinase inhibitors can successfully counteract angiogenesis in models of chronic liver disease, their clinical use might be limited by their potentially severe side effects, especially in a setting requiring chronic administration.…”

“…(8) In addition, we have recently reported elevated vascular cell adhesion molecule 1 (VCAM-1) serum levels in NAFLD patients, which might have clinical utility as a biomarker for the diagnosis of significant fibrosis. (9) However, although VEGF and multiple tyrosine kinase inhibitors can successfully counteract angiogenesis in models of chronic liver disease, (8,10,11) their clinical use might be limited by their potentially severe side effects, especially in a setting requiring chronic administration. Moreover, vascular alterations resulting from angiogenesis and endothelial dysfunction also promote monocyte infiltration, which in turn fuels NASH progression and stimulates angiogenesis.…”

The Influence of Nonalcoholic Fatty Liver Disease on the Platelet Hemostasis and Endothelial Function State in Patients with Stable Coronary Heart Disease

“…У свою чергу, активація тромбоцитів пов'язана з ендоте-ліальною дисфункцією та в подальшому -з ремо-делюванням судинної стінки [2]. Зокрема, збіль-шення рівня молекул адгезії сприяє проникненню лейкоцитів у судинну стінку та накопиченню в ній ліпідів, що відображає ступінь пошкодження ендо-теліальних клітин і порушення мікроциркуляції в тканинах [9,17]. Це викликає розвиток ендотеліаль-ної дисфункції, яка вважається одним із чинників розвитку ІХС.…”