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Hepatic Stellate Cell Contraction (HSC Contraction)

Target: HSC Contraction
Molecular classification: Cellular Process, Physiological Process, Targetable Process in Fibrosis

Overview

Hepatic stellate cell (HSC) contraction is a process where HSCs generate contractile force, regulating sinusoidal blood flow and contributing to liver fibrosis. Activated HSCs contract, narrowing sinusoids and increasing portal pressure. Contraction is driven by myosin II activation (Rho/Rho kinase pathway) and calcium signaling. Agonists like endothelin-1 and angiotensin-II promote contraction, while nitric oxide (NO) and other factors induce relaxation. HSC contraction is a therapeutic target for portal hypertension and liver fibrosis.

Other names: Stellate Cell ContractionHSC ContractilityLiver Stellate Cell Contraction

Mechanism of action

Modulation of HSC contractile machinery (myosin II activation via Rho/Rho kinase pathway) and/or calcium signaling. Augmentation of relaxation factors like nitric oxide.

Biological functions

Regulation of sinusoidal blood flowExtracellular matrix remodelingModulation of intrahepatic vascular resistanceVasoconstrictionVasodilation

Disease associations

Liver fibrosisCirrhosisPortal hypertension

Safety considerations

Potential for systemic hypotension with drugs targeting HSC contraction.Off-target effects of drugs affecting vascular tone.

Interacting drugs

Endothelin receptor antagonists

2 more in the full profile.

Biomarkers

Portal pressureHepatic venous pressure gradient (HVPG)Serum markers of fibrosis (e.g., hyaluronic acid, TIMP-1)

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