Journal
SEMINARS IN LIVER DISEASE
Volume 27, Issue 4, Pages 413-426Publisher
THIEME MEDICAL PUBL INC
DOI: 10.1055/s-2007-991517
Keywords
hepatic fibrogenesis; extracellular matrix; hepatic stellate cells; tissue inhibitors of metalloproteinases; signaling pathways
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Funding
- NIDDK NIH HHS [DK56621] Funding Source: Medline
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Hepatic fibrogenesis represents a wound-healing response of liver to a variety of insults, ultimately leading to decompensated cirrhosis in many patients and accounting for extensive morbidity and mortality worldwide. The net accumulation of extracellular matrix (ECM) in liver injury arises from increased synthesis by activated hepatic stellate cells and other hepatic fibrogenic cell types, as well as from bone marrow and circulating fibrocytes. Concurrently, degradation of ECM by matrix metalloproteinases (MMPs) fails to keep pace with increased synthesis, in part due to sustained expression of MMP inhibitors (e.g., tissue inhibitors of metalloproteinases). A growing list of circulating, paracrine, and autocrine mediators have been identified that amplify the fibrogenic response of liver. Combined with accelerating knowledge about signaling pathways and genetic determinants, major advances are anticipated in new diagnostics and therapies that will transform the care of patients with chronic liver diseases in the coming years.
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