BACKGROUND: Mitochondrial quality control (MQC) is crucial for maintaining mitochondrial fitness. We investigated MQC signaling in muscle of old hip-fractured patients. METHODS: Twenty-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 85years as the cut-off. The expression of a set of MQC signaling proteins was assayed in vastus lateralis muscle biopsies. RESULTS: The 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. CONCLUSIONS: Muscle 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.
BACKGROUND: Mitochondrial quality control (MQC) is crucial for maintaining mitochondrial fitness. We investigated MQC signaling in muscle of old hip-fracturedpatients. METHODS: Twenty-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 85years as the cut-off. The expression of a set of MQC signaling proteins was assayed in vastus lateralis muscle biopsies. RESULTS: The 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. CONCLUSIONS: Muscle 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.
Authors: Anna Picca; Sunil K Saini; Robert T Mankowski; George Kamenov; Stephen D Anton; Todd M Manini; Thomas W Buford; Stephanie E Wohlgemuth; Rui Xiao; Riccardo Calvani; Hélio José Coelho-Júnior; Francesco Landi; Roberto Bernabei; David A Hood; Emanuele Marzetti; Christiaan Leeuwenburgh Journal: Cells Date: 2020-12-02 Impact factor: 6.600