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Growth hormone secretagogues hexarelin and JMV2894 protect skeletal muscle from mitochondrial damages in a rat model of cisplatin-induced cachexia.

Sirago G, Conte E, Fracasso F, et al. Scientific reports. 2017.
Weak / noneAnimal (in vivo)Mentions: Hexarelin

Editor's note

In a rat model of cisplatin-induced cachexia (chemotherapy-associated muscle wasting), researchers reported that the growth hormone secretagogues hexarelin and JMV2894 counteracted mitochondrial damage in skeletal muscle. Cisplatin reduced mitochondrial biogenesis, mass, and fusion and increased reactive oxygen species; both secretagogues attenuated these changes. The work identifies mitochondrial protection as a plausible mechanism for GHS benefit in wasting. It is a single-model preclinical study, and hexarelin is evaluated alongside a novel compound rather than in isolation. Muscle mitochondrial markers are surrogate endpoints, not clinical outcomes. These are preclinical findings; human data are needed before any clinical conclusions can be drawn.

Plain-language abstract

Chemotherapy can cause cachexia, a wasting condition with severe muscle loss. Researchers studied this in rats treated with the chemotherapy drug cisplatin, and tested two growth-hormone-releasing peptides, hexarelin and an experimental one called JMV2894. Cisplatin damaged the energy-producing structures (mitochondria) in leg muscle, reducing their number and function and increasing harmful reactive oxygen molecules. Both peptides reduced this mitochondrial damage. The authors suggest protecting muscle mitochondria may be one way these peptides could help counter muscle wasting during chemotherapy. The abstract reports no adverse events. These are preclinical findings in rats; human studies would be needed before drawing any clinical conclusions.