Advanced chronic liver disease (aCLD) represents a major public health concern. aCLD is more prevalent and severe in the elderly, carrying a higher risk of decompensation. The socioeconomic and medical care improvement during the last decades has led to a relevant increase in the elderly population around the world. The incidence of aCLD increases dramatically with age, and is accompanied by worse prognosis, consequently aging has been defined as a major risk factor for the development of chronic liver conditions. Portal hypertension and liver fibrosis were exacerbated as a consequence of profound deregulations in the phenotype of the main hepatic cells: hepatocytes presented more extensive cell-death and poorer function, LSEC were further capillarized, HSC over-activated and macrophage infiltration was significantly increased. The gene expression signature of cirrhosis significantly differed comparing young and aged patients, indicating alterations in sinusoidal-protective pathways and confirming the pre-clinical observations. This study provides evidence that aCLD has a much-aggravated pathophysiology in aged individuals, and even more importantly, that aging may activate different or additional molecular mechanisms from those observed in young.

Source: Aging and Disease 2019, 10 (4): 684-698