Key result
Hepsin regulates liver metabolism and its deficiency lowers blood glucose in mouse models.
This review summarizes the biosynthesis, activation, and diverse physiological and pathological roles of the transmembrane serine protease hepsin.
Hepsin's metabolic role in mice merits targeted human studies; leaves open its viability as a glucose-lowering target.
Cell membrane-bound serine proteases are important in the maintenance of physiological homeostasis. Hepsin is a type II transmembrane serine protease highly expressed in the liver. Recent studies indicate that hepsin activates prohepatocyte growth factor in the liver to enhance Met signaling, thereby regulating glucose, lipid, and protein metabolism. In addition, hepsin functions in nonhepatic tissues, including the adipose tissue, kidney, and inner ear, to regulate adipocyte differentiation, urinary protein processing, and auditory function, respectively. In mouse models, hepsin deficiency lowers blood glucose, lipid, and protein levels, impairs uromodulin assembly in renal epithelial cells, and causes hearing loss. Elevated hepsin expression has also been found in many cancers. As a type II transmembrane protease, cell surface expression and zymogen activation are essential for hepsin activity. In this review, we discuss the current knowledge regarding hepsin biosynthesis, activation, and functions in pathobiology.
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Li et al. (2020) conducted a review in Hepsin pathobiology. Hepsin was evaluated. Hepsin is a multifunctional transmembrane serine protease that regulates metabolism in the liver and functions in nonhepatic tissues, with its deficiency in mouse models lowering blood glucose.
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