Abstract
Chronic liver damage can lead to hepatic fibrosis, a complex process caused by accumulation of extracellular matrix in the liver. Hepatic fibrosis is the final common pathway that may result in cirrhosis, and can ultimately require liver transplantation. The presence of obesity or overweight and the metabolic syndrome is a significant risk factor in the progression of this condition. In this paper, we discuss experimental and clinical evidence indicating the involvement of leptin, a major adipokine secreted by adipose tissue, in the modulation of fibrogenic process. In general, leptin has profibrogenic and proinflammatory actions, and it appears to control many fundamental aspects of the cellular and molecular biology related to hepatic fibrosis and its resolution. In particular, the effects of leptin on fibrogenic cells, endothelial cells, and macrophages are discussed.
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