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At the cellular level, the hypothesis focuses on how increased sinusoidal pressure is converted into mechanical stretch and mechano-signalling.
Hepatic stellate cells, liver sinusoidal endothelial cells and hepatocytes are positioned within a mechanically sensitive perisinusoidal environment. Congestion, inflammation, cell swelling and altered flow can increase local pressure and stretch. Persistent mechanical stimulation may then promote stellate-cell activation, extracellular matrix production and vascular remodeling.
This perspective connects hemodynamics with cellular fibrogenesis and complements molecular models that explain fibrosis primarily through inflammatory or toxic signalling.
