The muscle RING-finger protein-1 (MuRF1) is an E3 ubiquitin ligase expressed in skeletal and cardiac muscle tissues and it plays important roles in muscle remodeling. Upregulation of MuRF1 gene transcription participates in skeletal muscle atrophy, on contrary downregulation of protein expression leads to cardiac hypertrophy[1]. EMBL(MuRF1-IN-1) is a MuRF1 inhibitor that attenuates skeletal muscle atrophy and dysfunction in cardiac cachexi. EMBL was able to attenuate in vivo skeletal muscle atrophy and contractile dysfunction in a mouse model of cardiac cachexia. Whereby myotube atrophy induced by the synthetic glucocorticoid DEX was abolished following treatment with EMBL. The compound-induced attenuation of muscle wasting both in vivo and in vitro was associated with reduced levels of MuRF1 expression, while additional proteome analyses revealed a protection of de novo protein synthesis and a down-regulation in apoptosis. EMBL directed to MuRF1 central attenuated in vivo muscle wasting and contractile dysfunction in cardiac cachexia by mechanisms that involved a protection of muscle protein de novo synthesis and a down-regulation in apoptosis[2]. Treatment with EMBL in CHF mice had beneficial effects on the diaphragm: contractile function was protected, while mitochondrial enzyme activity and up-regulation of the MuRF1 and MuRF2 was attenuated after infarct[3].
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