التفاصيل البيبلوغرافية
| العنوان: |
Hepatic stellate cells and alcoholic liver disease |
| المؤلفون: |
Vera,M., Nieto,N. |
| المصدر: |
Revista Española de Enfermedades Digestivas v.98 n.9 2006 |
| بيانات النشر: |
Sociedad Española de Patología Digestiva |
| سنة النشر: |
2006 |
| المجموعة: |
SciELO España (Scientific Electronic Library Online) |
| مصطلحات موضوعية: |
Hepatic stellate cells, Collagen I, Alcoholic liver disease, Fibrosis, Extracellular matrix, Reactive oxigen species |
| الوصف: |
Liver fibrosis represents a significant health problem worldwide for which no effective therapy exists. A great deal of research has been carried out to understand the molecular mechanisms responsible for the development of liver fibrosis. Activated stellate cells are the primary cell type responsible for the production of collagen I, the key protein involved in the development of liver fibrosis. Excessive deposition of collagen I occurs along with impaired extracellular matrix remodeling. Following a fibrogenic stimulus stellate cells transform into an activated collagen type I-producing cell. Numerous changes in gene expression are associated with stellate cell activation, including the induction of several intracellular signaling cascades, which help maintain the activated phenotype and control the fibrogenic and proliferative state of the cell. Activation of stellate cells is mediated by factors released from hepatocytes and Kupffer cells as they produce reactive oxygen species, nitric oxide, cytokines, growth factors, and cyclooxygenase and lipoxygenase metabolites, which provide pivotal paracrine effects in the liver milieu. Inhibition of stellate cell activation, proliferation, and the increased production of extracellular matrix (i.e. collagen type I) are therefore crucial steps for intervention in hepatic fibrogenesis. |
| نوع الوثيقة: |
article in journal/newspaper |
| وصف الملف: |
text/html |
| اللغة: |
English |
| الإتاحة: |
https://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1130-01082006000900005Test |
| رقم الانضمام: |
edsbas.17A5EEDD |
| قاعدة البيانات: |
BASE |
