scholarly journals Placental growth factor silencing ameliorates liver fibrosis and angiogenesis and inhibits activation of hepatic stellate cells in a murine model of chronic liver disease

2017 ◽  
Vol 21 (10) ◽  
pp. 2370-2385 ◽  
Author(s):  
Xi Li ◽  
Qun-Yan Yao ◽  
Hong-Chun Liu ◽  
Qian-Wen Jin ◽  
Bei-Li Xu ◽  
...  
Keyword(s):  
Liver Disease ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Chronic Liver Disease ◽  
Murine Model ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Placental Growth Factor ◽  
Chronic Liver

scholarly journals Activated Hepatic Stellate Cells Express Keratinocyte Growth Factor in Chronic Liver Disease

2004 ◽  
Vol 165 (4) ◽  
pp. 1233-1241 ◽  
Author(s):  
Heike Steiling ◽  
Marcus Mühlbauer ◽  
Frauke Bataille ◽  
Jürgen Schölmerich ◽  
Sabine Werner ◽  
...  
Keyword(s):  
Liver Disease ◽  
Growth Factor ◽  
Chronic Liver Disease ◽  
Hepatic Stellate Cells ◽  
Keratinocyte Growth Factor ◽  
Stellate Cells ◽  
Chronic Liver ◽  
Activated Hepatic Stellate Cells

scholarly journals Integration of miRNA‐regulatory networks in hepatic stellate cells identifies TIMP3 as a key factor in chronic liver disease

2020 ◽  
Vol 40 (8) ◽  
pp. 2021-2033 ◽  
Author(s):  
Fida Azar ◽  
Kevin Courtet ◽  
Bassil Dekky ◽  
Dominique Bonnier ◽  
Olivier Dameron ◽  
...  
Keyword(s):  
Liver Disease ◽  
Chronic Liver Disease ◽  
Hepatic Stellate Cells ◽  
Regulatory Networks ◽  
Stellate Cells ◽  
Chronic Liver ◽  
Key Factor

scholarly journals Serum cytokines, adipokines and ferritin for non-invasive assessment of liver fibrosis in chronic liver disease: a systematic review

2019 ◽  
Vol 57 (5) ◽  
pp. 577-610 ◽  
Author(s):  
Seyyed Mortaza Haghgoo ◽  
Heidar Sharafi ◽  
Seyed Moayed Alavian
Keyword(s):  
Chronic Hepatitis ◽  
Liver Disease ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Chronic Liver Disease ◽  
Serum Levels ◽  
Chronic Liver ◽  
Major Health Problem ◽  
Non Invasive ◽  
Tgf Β1

AbstractChronic liver disease (CLD) is a major health problem worldwide. Non-alcoholic fatty liver disease (NAFLD), chronic hepatitis C (CHC), chronic hepatitis B (CHB), and alcoholic liver disease (ALD) are the most common etiologies of CLD. Liver biopsy is the gold standard for assessment of liver fibrosis, however, it is an invasive method. This review attempts to evaluate the usefulness of serum adiponectin, serum leptin, serum ferritin, serum transforming growth factor-β1 (TGF-β1), and serum platelet derived growth factor-BB (PDGF-BB) as non-invasive markers in the diagnosis of liver fibrosis/cirrhosis. A systematic search in MEDLINE, Web of Science, Scopus, and local databases was performed to identify articles published in English or Persian as of November 2017. Studies conducted among CLD patients, with biopsy proven fibrosis/cirrhosis, and providing sufficient details of patients’ clinicopathological characteristics were included. In the 95 studies included, there were a total of 15,548 CLD patients. More than 83% of studies were carried out in Asia and Europe. The relationship between liver fibrosis/cirrhosis and serum levels of ferritin, adiponectin, leptin, TGF-β1, and PDGF-BB was assessed in 42, 33, 27, nine, and three studies, respectively. Serum levels of the markers, particularly ferritin, could successfully predict liver fibrosis/cirrhosis, however, these data might not be clinically replicated and further studies are needed.

scholarly journals Role of Smad3 in platelet-derived growth factor-C-induced liver fibrosis

2016 ◽  
Vol 310 (6) ◽  
pp. C436-C445 ◽  
Author(s):  
Jung Il Lee ◽  
Jocelyn H. Wright ◽  
Melissa M. Johnson ◽  
Renay L. Bauer ◽  
Kristina Sorg ◽  
...  
Keyword(s):  
Liver Disease ◽  
Growth Factor ◽  
Liver Fibrosis ◽  
Signaling Pathways ◽  
Chronic Liver Disease ◽  
Molecular Mechanisms ◽  
Chronic Liver ◽  
Platelet Derived Growth Factor ◽  
Tgfβ Signaling ◽  
Factor C

Chronic liver injury leads to fibrosis and cirrhosis. Cirrhosis, the end stage of chronic liver disease, is a leading cause of death worldwide and increases the risk of developing hepatocellular carcinoma. Currently, there is a lack of effective antifibrotic therapies to treat fibrosis and cirrhosis. Development of antifibrotic therapies requires an in-depth understanding of the cellular and molecular mechanisms involved in inflammation and fibrosis after hepatic injury. Two growth factor signaling pathways that regulate liver fibrosis are transforming growth factor-β (TGFβ) and platelet-derived growth factor (PDGF). However, their specific contributions to fibrogenesis are not well understood. Using a genetic model of liver fibrosis, we investigated whether the canonical TGFβ signaling pathway was necessary for fibrogenesis. PDGF-C transgenic ( PDGF-C Tg) mice were intercrossed with mice that lack Smad3, and molecular and histological fibrosis was analyzed. PDGF-C Tg mice that also lacked Smad3 had less fibrosis and improved liver lobule architecture. Loss of Smad3 also reduced expression of collagen genes, which were induced by PDGF-C, but not the expression of genes frequently associated with hepatic stellate cell (HSC) activation. In vitro HSCs isolated from Smad3-null mice proliferated more slowly than cells from wild-type mice. Taken together, these findings indicate that PDGF-C activates TGFβ/Smad3 signaling pathways to regulate HSC proliferation, collagen production and ultimately fibrosis. In summary, these results suggest that inhibition of both PDGF and TGFβ signaling pathways may be required to effectively attenuate fibrogenesis in patients with chronic liver disease.

Sign in / Sign up

Export Citation Format

Share Document