ArticleJournal of translational medicine2019
Clusterin silencing restores myoblasts viability and down modulates the inflammatory process in osteoporotic disease.
Article in Journal of translational medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Associations of circulating apolipoprotein J and myostatin with sarcopenia in older adults with and without type 2 diabetes: a cross-sectional study.Frontiers in endocrinology · 2025Article
- Clusterin: structure, function and roles in disease.International journal of medical sciences · 2025Review
- Small interfering RNAs in the management of human osteoporosis.British medical bulletin · 2023Review
- Post-translational regulation of muscle growth, muscle aging and sarcopenia.Journal of cachexia, sarcopenia and muscle · 2023Review
- Article
- Roles of constitutively secreted extracellular chaperones in neuronal cell repair and regeneration.Neural regeneration research · 2023Review
- Oligonucleotide Therapeutics for Age-Related Musculoskeletal Disorders: Successes and Challenges.Pharmaceutics · 2023Review
- Enhanced external counterpulsation improves dysfunction of forearm muscle caused by radial artery occlusion.Frontiers in cardiovascular medicine · 2023Article
- The therapeutic and prognostic role of clusterin in diverse musculoskeletal diseases: a mini review.Physiological research · 2022Review
- Clusterin negatively modulates mechanical stress-mediated ligamentum flavum hypertrophy through TGF-β1 signaling.Experimental & molecular medicine · 2022Article
- Deregulated Clusterin as a Marker of Bone Fragility: New Insights into the Pathophysiology of Osteoporosis.Genes · 2022Article
- Integrated genomic and proteomic analyses identify stimulus-dependent molecular changes associated with distinct modes of skeletal muscle atrophy.Cell reports · 2021Article
- Serum complement proteomics reveal biomarkers for hypertension disorder of pregnancy and the potential role of Clusterin.Reproductive biology and endocrinology : RB&E · 2021Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTargeting new molecular pathways leading to Osteoporosis (OP) and Osteoarthritis (OA) is a hot topic for drug discovery. Clusterin (CLU) is a glycoprotein involved in inflammation, proliferation, cell death, neoplastic disease, Alzheimer disease and aging. The present study focuses on the expression and the role of CLU in influencing the decrease of muscle mass and fiber senescence in OP-OA condition.
methodsVastus lateralis muscle biopsies were collected from 20 women with OP undergoing surgery for fragility hip fracture and 20 women undergoing arthroplasty for hip osteoarthritis.
resultsWe found an overexpression of CLU in degenerated fibers in OP closely correlated with interleukin 6 (IL6) and histone H4 acetylation level. Conversely, in OA muscle tissues we observed a weak expression of CLU but no nuclear histone H4 acetylation. Ex vivo studies on isolated human myoblasts confirmed CLU overexpression in OP as compared to OA (p < 0.001). CLU treatment of isolated OP and OA myoblasts showed: modulation of proliferation, morphological changes, increase of histone H4 acetylation and induction of myogenin (MYOG) activation in OP myoblast only. In OP condition, functional knockdown of CLU by siRNA restores proliferative myoblasts capability and tissue damage repair, carried out by an evident upregulation of Transglutaminase 2 (TGM2). We also observed downmodulation of CX3CR1 expression with consequent impairing of the inflammatory infiltrate recruitment.
conclusionsResults obtained suggest a potential role of CLU in OP by influencing myoblasts terminal differentiation, epigenetic regulation of muscle cell differentiation and senescence. Moreover, CLU silencing points out its role in the modulation of tissue damage repair and inflammation, proposing it as a new diagnostic marker for muscle degeneration and a potential target for specific therapeutic intervention in OP related sarcopenia.
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