Identification of novel targets for the diagnosis and treatment of liver fibrosis
| Autor: | Giuseppe A.G. Lombardo, Rosario Caltabiano, Paolo Fagone, Aurora Pesce, Santa Mammana, Antonio Pesce, Katia Mangano, Alexandra Giorlandino, Ferdinando Nicoletti, Eugenio Cavalli, Teresa Rosanna Portale, Stefano Puleo, Marinella Coco |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Liver Cirrhosis
Pathology medicine.medical_specialty Cell type Cell Down-Regulation Biology Extracellular matrix Drug Discovery Genetics medicine Humans Gene Regulatory Networks Molecular Targeted Therapy Liver injury General Medicine Cell cycle medicine.disease Up-Regulation medicine.anatomical_structure Gene Ontology Liver Hepatic stellate cell Cancer research Hepatic fibrosis Myofibroblast |
| Zdroj: | International journal of molecular medicine. 36(3) |
| ISSN: | 1791-244X |
| Popis: | Liver fibrosis is characterized by the excessive deposition of extracellular matrix (ECM) in the hepatic parenchyma and represents an intrinsic response to chronic injury, maintaining organ integrity when extensive necrosis or apoptosis occurs. Hepatic stellate cells (HSCs) are the major cell type responsible for liver fibrosis. Following liver injury, HSCs become activated and transdifferentiate into myofibroblasts (MFBs) that lead to intrahepatic ECM accumulation. In the present study, we performed a meta‑analysis of datasets which included whole-genome transcriptional data on HSCs in the quiescent and activated state from two different rodent species and identified commonly regulated genes. Several of the genes identified, including ECM components, metalloproteinases and growth factors, were found to be well‑known markers for HSC activation. However, other significant genes also appeared to play important roles in hepatic fibrosis. The elucidation of the molecular events underlying HSC activation may be key to the identification of potential novel pharmacological targets for the prevention and treatment of liver fibrosis. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|