Aging is a key risk factor for the development of liver fibrosis, mainly in hepatitis, which can lead to portal hypertension and cirrhosis.

Elderly people continue to increase worldwide and are predominantly at risk for yielding to liver failure owing to the declines in reformative capacity, reduced survival post-liver transplantation, and inclinations to grow inflammation and fibrosis

Macrophages performance a crucial role in the homeostatic functions of the liver as well as in disease states and are amongst the greatest widely studied immune cells in the liver. The occurrence and severity of many chronic liver diseases increases with age, including alcoholic hepatitis, non-alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma.

Macrophage inhabitants in the gut, spleen, and lungs are continuously replenished by monocyte input throughout adulthood. Within the past decade, the heterogeneity of hepatic macrophages, i.e., Kupffer cells and monocyte-derived macrophages (mMØs), has become an emerging topic in hepatology. Fate tracing experiments in the brain first determined that resident microglia are established prenatally and maintained independently from monocyte input, which was later translated to the liver.

Liver transplantation is the standard treatment for patients with end stage liver disease. Elderly with liver cirrhosis needing transplantation has grown over the past 20 years and is likely to grow further modulating macrophage polarization has been considered a ambiguous sword, and the appearance of liver fibrosis or HCC would need to be closely monitored. Treatment of the primary caters of age-associated liver diseases such as alcohol consumption, visceral and ectopic fat accumulation, or deficits in mitochondrial capacity and other age-related mechanisms, is as essential as targeting the provocative symptoms to combat these age-related liver diseases.

Source: Front Immunol. 2018; 9: 2795