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[Comment] Chronic liver disease: scavenger hunt for novel therapies

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Scavenger receptors mediate distinct immune pathways in chronic liver injury

Chronic liver injury is associated with hepatocyte damage and metabolic stress, which cumulatively lead to the release of danger-associated molecular patterns (DAMPs), including oxidised LDLs (oxLDLs; red dots in figure ) and the activation of hepatic stellate cells (HSC). DAMPs are recognised by hepatic sinusoidal endothelial cells (HSEC) and liver macrophages (MACROs) through surface receptors including scavenger receptors—eg, stabilin-1, CD36, and macrophage scavenger receptor-1 (MSR-1). In the context of chronic liver injury, stabilin-1 promotes immunosuppressive pathways, including suppression of chemokine CCL3 secretion and recruitment of regulatory T cells, whereas CD36 and MSR-1 promote proinflammatory immune cell recruitment. Therefore, targeted therapies could be developed for hepatocellular cancer by targeting stabilin-1, and for liver fibrosis by targeting CD36 and MSR-1, the pathways of which could both potentially be blocked with antibodies or small molecule inhibitors.

Chronic liver disease (CLD) is a major cause of global mortality and morbidity. However, therapeutic breakthroughs have been made in the field of viral hepatitis, with the development of direct-acting antiviral agents (DAAs) to treat hepatitis C virus infection.1 Despite this breakthrough, the incidence of liver disease continues to rise, driven in particular by the increase in obesity-related fatty-liver disease and the consequences of excess alcohol consumption.2 Patients with CLD are at an increased risk of developing progressive liver fibrosis, cirrhosis, and liver failure.

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