A fibrous liver is characterized by the excessive accumulation of extracellular matrix (ECM) proteins, such as collagen, resulting from chronic injury and hepatic stellate cell (HSC) activation into myofibroblasts. This scarring distorts the liver's lobular architecture, replacing functional hepatocytes with fibrous bands, increasing collagen content up to six times, and causing nodular regeneration.
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Key Anatomical and Histological Changes
- Fibrous Tissue Accumulation: Chronic injury, such as from alcohol, hepatitis, or steatosis, triggers HSCs in the space of Disse to transform into myofibroblasts, which produce excess ECM.
- Structural Distortion: Normal hexagonal lobules are replaced by distorted, scarred tissue, leading to portal-central vascular shunts and reduced perfusion of hepatocytes.
- Vascular Changes: The liver develops a thickened basement membrane (capillarization of sinusoids) and increased vascular resistance.
- Cirrhosis: Progressive, widespread scarring (fibrosis) bridges vascular structures, turning the liver into a nodular, hard, or "fibrous" organ.
Glisson's Capsule: The fibrous outer capsule may appear thickened in advanced stages.
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Functional Impact
- Portal Hypertension: The altered vascular anatomy increases pressure in the portal vein.
Liver Failure: The reduction of functional parenchyma causes impairment of detoxification, synthesis, and metabolic functions.
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Reversibility
Fibrosis can sometimes be reversed if the underlying cause is addressed early, as Matrix Metalloproteinases (MMPs) can degrade the accumulated collagen