Cardiac hypertrophy is inhibited by antagonism of ADAM12 processing of HB-EGF: Metalloproteinase inhibitors as a new therapy

By M. Asakura, M. Kitakaze, S. Takashima, Y. Liao, F. Ishikura, Tsuyoshi Yoshinaka, H. Ohmoto, K. Node, K. Yoshino, H. Ishiguro and 8 more. 2002

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A Disintegrin and Metalloproteinase (ADAM) and ADAM with Thrombospondin Motifs (ADAMTS) Family in Vascular Biology and Disease (2019, background): “ADAM-12L can mediate cardiomyocyte hypertrophy by controlling the shedding of HBEGF [71, 72], and Notch signal pathway [73], and thereby regulates the disease progression [73, 74].”
Distinct roles for ADAM10 and ADAM17 in ectodomain shedding of six EGFR ligands (2004, background): “Furthermore, three other ADAMs (9, 10, and 12) had been implicated in HB-EGF shedding (Izumi et al., 1998; Asakura et al., 2002; Lemjabbar and Basbaum, 2002), raising questions about their individual contributions to HB-EGF release.”
ErbB receptors: directing key signaling networks throughout life. (2004, background): “Recently, the ADAMs have been shown to play pivotal roles in proligand cleavage following treatment with GPCR agonists (12, 61, 62).”
Phenotypic Analysis of Meltrin α (ADAM12)-Deficient Mice: Involvement of Meltrin α in Adipogenesis and Myogenesis (2003, background): “Recent studies with metalloprotease inhibitors have implicated metalloproteases in the ectodomain shedding of HB-EGF (1).”