期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 600, 期 11, 页码 2579-2612出版社
WILEY
DOI: 10.1113/JP281135
关键词
fibrosis; fibroblasts; liver; pancreas; stellate cells
资金
- National Science Centre of Poland (Narodowe Centrum Nauki, NCN) [2019/33/B/NZ3/02578]
- PRELUDIUM projects from NCN [2021/41/N/NZ4/03959, 2021/41/N/NZ3/04320]
- BioS Priority Research Area mini grant [U1U/P03/NO/14.89]
- ETIUDA PhD scholarship from NCN [U1U/P03/NO/14.89]
Fibrosis is a manifestation of chronic diseases that results in excessive deposition of extracellular matrix, compromising normal tissue functions. Hepatic and pancreatic stellate cells are the main cellular mediators of fibrosis, undergoing phenotypic switch in response to stimuli. Current scientific research focuses on investigating the pathogenesis of fibrosis and potential therapies.
Disorders such as pancreatic or hepatic fibrosis are a cruel reminder that disruption of the delicate physiological balance could result in severe pathological consequences. Fibrosis is usually associated with chronic diseases and manifests itself as excessive deposition of the extracellular matrix, which gradually leads to the replacement of the cellular components by fibrotic lesions, significantly compromising normal tissue functions. The main cellular mediators of fibrosis are different populations of tissue fibroblasts, predominantly hepatic and pancreatic stellate cells in the liver and pancreas, respectively. These cells undergo a phenotypic switch in response to (bio)chemical or physical stimuli and acquire a myofibroblast-like phenotype characterised by increased contractile and adhesive properties, elevated expression of certain cytoskeletal and membrane proteins, and prominent production of extracellular matrix components. In the past few decades, a substantial scientific effort has been undertaken to investigate the pathogenesis of fibrosis. Here, cellular mechanisms of hepatic and pancreatic fibrosis, their aetiological factors, associated diseases and prospective therapies are discussed. New therapies against fibrosis are likely to be focused on regulation of hepatic/pancreatic stellate cell physiology as well as normalisation of the organ mechanostasis.
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