Association between myocyte quality control signaling and sarcopenia in old hip-fractured patients: Results from the sarcopenia in hip fracture (Shift) exploratory study
Abstract
Background Sarcopenia has been proposed as a potentially amenable factor impacting the clinical outcomes of hip-fractured elderly. The identification of specific biological targets is therefore crucial to developing pharmacological interventions against age-related muscle wasting. The present work reports promising preliminary data on the association between alterations of myocyte quality control (MQC) signaling and sarcopenia in old patients with hip fracture.Methods Twenty-five elderly hip-fractured patients (20 women and 5 men; mean age 84.9±1.65years) were enrolled as part of the Sarcopenia in HIp FracTure (SHIFT) study. Intraoperative biopsies of the vastus lateralis muscle were obtained and assayed for the expression of a set of MQC signaling proteins. The presence of sarcopenia was established according to the European Working Group on Sarcopenia in Older People (EWGSOP) criteria, with bioelectrical impedance analysis used for fat-free mass estimation.Results Sarcopenia was identified in 10 patients (40%). Protein expression of the mitochondrial fusion factor mitofusin (Mfn) 2 and the autophagy mediator microtubule-associated protein 1 light chain 3B (LC3B) was significantly lower in patients with sarcopenia compared with non-sarcopenic controls. No differences between groups were observed for Mfn1, optic atrophy protein 1 (OPA1), fission protein 1 (Fis1), and the master regulator of mitochondrial biogenesis peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α).Conclusion Data from this exploratory study show that a reduced expression of the mitochondrial fusion factor Mfn2 and the autophagy mediator LC3B is associated with sarcopenia in old hip-fractured patients. Future larger-scale studies are needed to corroborate these preliminary findings and determine whether MQC pathways may be targeted to improve muscle health and promote functional recovery in old patients with hip fracture.
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Reduced expression levels of OPA1 and MFN2 have been described in the skeletal muscle of elderly individuals.
“For instance, reduced expression levels of OPA1 (71) and MFN2 (83) have been described in the skeletal muscle of elderly individuals.”
From From mitochondria to sarcopenia: role of 17β-estradiol and testosterone (2023) · cites this paper as [83]
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- Authors
- Marzetti, E., Calvani, R., Lorenzi, M., Tanganelli, F., Picca, A., Bossola, M., Menghi, A., Bernabei, R., & Landi, F.
- Affiliations
- Università Cattolica del Sacro Cuore (IT)
- Corresponding author
- Calvani, Riccardo
- ORCID
- Venue
- Experimental Gerontology
- Publisher
- Elsevier BV
- Published
- 2016-07
- Volume
- 80
- Pages
- 1-5
- ISSN
- 0531-5565 (ISSN-L)
- OpenAlex
- W2325467234
- Cited by
- 58
- References
- 19
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 5 · 2021: 8 · 2020: 8 · 2019: 3 · 2018: 8 · 2017: 6 · 2016: 3
- FWCI
- 5.36
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Experimental Gerontology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Innovative Medicines Initiative – Joint Undertaking (IMI-JU #115621)
- Italian Ministry of Education, Universities and Research (MIUR D3.2 2013)
- Centro Studi Achille e Linda Lorenzon
- Topics
- Health Sciences › Medicine › Physiology › Nutrition and Health in Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- sarcopenia, hip fracture, older adults, mitochondrial fusion, mitofusin 2, autophagy, LC3B, muscle atrophy, vastus lateralis, mitochondrial biogenesis, PGC-1α, OPA1, Fis1
- MeSH terms
- Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, Aged, 80 and over, Atrophy, Autophagy, Organelle Biogenesis, Female, Hip Fractures, Humans, Italy, Male, Membrane Proteins, Microtubule-Associated Proteins, Muscles, Signal Transduction, GTP Phosphohydrolases, Mitochondrial Proteins, Mitochondrial Membrane Transport Proteins, Sarcopenia, Mitochondrial Dynamics
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