From the muscle hypothesis to a muscle solution?

摘要

In this issue, ESC Heart Failure publishes an extremely interesting paper.1 Sabbah and colleagues tested elamipretide(ELAM), a peptide that targets mitochondria, thereby possiblyaffecting many organs, but clearly with skeletal muscle also akey target. In their well-established and characterized caninemodel of chronic intracoronary microembolization-inducedheart failure (HF), 3 months of ELAM therapy led to a shiftin type 1 to type 2 fibres, restoring the balance towards normal. In addition, skeletal muscle mitochondrial function in theHF dogs was abnormal in terms of ADP-dependent mitochondrial respiration, membrane potential, permeability transitionpore, stimulated ATP synthesis, and cytochrome c oxidase activity; and all of these were near normalized by short-termin vitro application of ELAM. Sabbah and colleagues concludethat ‘ELAM, previously shown to positively influence mitochondrial function of the failing heart, can also positivelyimpact mitochondrial function of skeletal muscle and potentially help restore skeletal muscle function and improve exercise tolerance'.