Mitochondrial dynamics signaling is shifted toward fusion in muscles of very old hip-fractured patients: Results from the Sarcopenia in HIp FracTure (SHIFT) exploratory study


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Abstract

BackgroundMitochondrial quality control (MQC) is crucial for maintaining mitochondrial fitness. We investigated MQC signaling in muscle of old hip-fractured patients.MethodsTwenty-three patients, enrolled in the Sarcopenia in HIp FracTure (SHIFT) study, were categorized into old (OL; n = 8) and very old groups (VOL; n = 15) using 85 years as the cut-off. The expression of a set of MQC signaling proteins was assayed in vastus lateralis muscle biopsies.ResultsThe content of lysosome-associated membrane protein 2, microtubule-associated protein 1 light chain 3B, optic atrophy protein 1, fission protein 1 (Fis1), peroxisome proliferator-activated receptor-γ coactivator-1α, and forkhead box O3 was unvaried between groups. Conversely, the protein expression of mitofusin 2 (Mfn2) as well as the fusion index (Mfn2/Fis1) was increased in VOL patients.ConclusionsMuscle mitochondrial dynamics appear to be shifted toward fusion in very advanced age. Whether this phenomenon represents an adaptation to cope with age-dependent mitochondrial dysfunction warrants further investigation.HighlightsMitochondrial quality control (MQC) is essential for maintaining organelle fitness.Alterations of MQC have been described in several conditions, including aging.Muscle mitochondrial dynamics appear to be shifted toward fusion in very old age.Autophagy and mitochondriogenesis signaling is similar in old and very old patients.Up-regulation of fusion may serve to buffer the increased load of mtDNA mutations.

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