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Although agonism of the glucagon receptor has emerged as a promising approach for increasing catabolic metabolism, an elevated heart rate, hepatic glucose production and concerns about lean mass loss, might restrict its application, especially for T2DM (95)

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These results suggest that reduced homocysteine causes protein thiol homocysteinylation that may induce smooth muscle cell proliferation by binding to a redox receptor and that may exacerbate atherosclerotic lesion formation by inducing collagen expression (Tyagi, 1998)

TAM's interaction with tumor cells has been demonstrated to result in increased VEGFA production, consequent angiogenesis, and tumor aggressiveness