Abstract:
:Chemotherapy can cause cachexia, which consists of weight loss associated with muscle atrophy. The exact mechanisms underlying this skeletal muscle toxicity are largely unknown and co-therapies to attenuate chemotherapy-induced side effects are lacking. By using a rat model of cisplatin-induced cachexia, we here characterized the mitochondrial homeostasis in tibialis anterior cachectic muscle and evaluated the potential beneficial effects of the growth hormone secretagogues (GHS) hexarelin and JMV2894 in this setting. We found that cisplatin treatment caused a decrease in mitochondrial biogenesis (PGC-1α, NRF-1, TFAM, mtDNA, ND1), mitochondrial mass (Porin and Citrate synthase activity) and fusion index (MFN2, Drp1), together with changes in the expression of autophagy-related genes (AKT/FoxO pathway, Atg1, Beclin1, LC3AII, p62) and enhanced ROS production (PRX III, MnSOD). Importantly, JMV2894 and hexarelin are capable to antagonize this chemotherapy-induced mitochondrial dysfunction. Thus, our findings reveal a key-role played by mitochondria in the mechanism responsible for GHS beneficial effects in skeletal muscle, strongly indicating that targeting mitochondrial dysfunction might be a promising area of research in developing therapeutic strategies to prevent or limit muscle wasting in cachexia.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Sirago G,Conte E,Fracasso F,Cormio A,Fehrentz JA,Martinez J,Musicco C,Camerino GM,Fonzino A,Rizzi L,Torsello A,Lezza AMS,Liantonio A,Cantatore P,Pesce Vdoi
10.1038/s41598-017-13504-ysubject
Has Abstractpub_date
2017-10-12 00:00:00pages
13017issue
1issn
2045-2322pii
10.1038/s41598-017-13504-yjournal_volume
7pub_type
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