Abstract
Liver fibrosis is a common wound healing response to chronic liver injury of all causes, and its end-stage cirrhosis is responsible for high morbidity and mortality worldwide. Fibrosis results from prolonged parenchymal cell apoptosis and necrosis associated with an inflammatory reaction that leads to recruitment of immune cells, activation and accumulation of fibrogenic cells, and extracellular matrix accumulation. The fibrogenic process is driven by hepatic myofibroblasts, that mainly derive from hepatic stellate cells undergoing a transdifferentiation from a quiescent, lipid-rich into a fibrogenic myofibroblastic phenotype, in response to paracrine/autocrine signals produced by neighbouring inflammatory and parenchymal cells. Autophagy is an important regulator of liver homeostasis under physiological and pathological conditions. This review focuses on recent findings showing that autophagy is a novel, but complex, regulatory pathway in liver fibrosis, with profibrogenic effects relying on its direct contribution to the process of hepatic stellate cell activation, but with antifibrogenic properties via indirect hepatoprotective and anti-inflammatory properties. Therefore, cell-specific delivery of drugs that exploit autophagic pathways is a prerequisite to further consider autophagy as a potential target for antifibrotic therapy.
Highlights
Liver fibrosis is defined by the excessive accumulation of extracellular matrix in response to chronic injury regardless of the cause
Autophagy is an important regulator of liver homeostasis under physiological conditions [7,8,9]
The sequestration of mitochondria and protein aggregates mainly relies on the selective recognition of cargoes by autophagy adaptors, such as SQSTM1/p62, that bridge the cargoes to the autophagic machinery [3, 4]
Summary
Liver fibrosis is defined by the excessive accumulation of extracellular matrix in response to chronic injury regardless of the cause. BioMed Research International priority goal for hepatologists In this respect, recent data have conclusively established, both in experimental models and in cohort studies, that eradication or efficient control of the cause of liver disease may be associated with regression of fibrosis and early stage cirrhosis [2]. Recent data have conclusively established, both in experimental models and in cohort studies, that eradication or efficient control of the cause of liver disease may be associated with regression of fibrosis and early stage cirrhosis [2] This goal cannot be achieved in several instances, which justifies past and ongoing massive efforts to identify potential therapeutic antifibrotic targets
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