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Although its selectivity is not necessarily superior to existing inhibitors, DLK1 competes with MSTN for binding to ActRIIB and promotes muscle regeneration through modulation of SMAD2/3 and Notch signaling pathways.[88] However, to date, no clinical trials have investigated DLK1 activation or overexpression as a strategy to promote muscle growth, although such studies may offer promising therapeutic opportunities for the management of metabolic disorders
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