ArticleThe Journal of biological chemistry2015
Impaired bone homeostasis in amyotrophic lateral sclerosis mice with muscle atrophy.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Reduced osteogenic factors and early osteoblast senescence in SOD1(G93A) ALS mouse model.JCI insight · 2026Article
- Absence of Neuromuscular Dysfunction in Mice with Gut Epithelium-Restricted Expression of ALS Mutation hSOD1Biomolecules · 2026Article
- Antibody-Based PET Imaging of Misfolded Superoxide Dismutase 1 in an Amyotrophic Lateral Sclerosis Mouse Model.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2025Article
- Wnt/β-catenin signaling pathway as an important mediator in muscle and bone crosstalk: A systematic review.Journal of orthopaedic translation · 2024Review
- Amyotrophic lateral sclerosis and osteoporosis: a two-sample Mendelian randomization study.Frontiers in aging neuroscience · 2023Article
- Review
- ROS-Mediated Enamel Formation Disturbance Characterized by Alternative Cervical Loop Cell Proliferation and Downregulation of RhoA/ROCK in Ameloblasts.Oxidative medicine and cellular longevity · 2022Article
- Kindlin-2 deletion in osteoprogenitors causes severe chondrodysplasia and low-turnover osteopenia in mice.Journal of orthopaedic translation · 2022Article
- The Dual Effects of Reactive Oxygen Species on the Mandibular Alveolar Bone Formation in SOD1 Knockout Mice: Promotion or Inhibition.Oxidative medicine and cellular longevity · 2021Article
- Amyotrophic lateral sclerosis (ALS) and the endocrine system: Are there any further ties to be explored?Aging brain · 2021Review
- Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice.Signal transduction and targeted therapy · 2020Article
- Kindlin-2 modulates MafA and β-catenin expression to regulate β-cell function and mass in mice.Nature communications · 2020Article
- Poor Bone Quality in Patients With Amyotrophic Lateral Sclerosis.Frontiers in neurology · 2020Article
- Focal adhesion protein Kindlin-2 regulates bone homeostasis in mice.Bone research · 2020Article
- LIM domain proteins Pinch1/2 regulate chondrogenesis and bone mass in mice.Bone research · 2020Article
- Effects of Neurological Disorders on Bone Health.Frontiers in psychology · 2020Review
- Temporal evolution of the microbiome, immune system and epigenome with disease progression in ALS mice.Disease models & mechanisms · 2019Article
- Article
- Risk of osteoporosis in patients with chronic inflammatory neuropathy- a population-based cohort study.Scientific reports · 2019Article
- Dysregulated mitochondrial CaArchives of biochemistry and biophysics · 2019Review
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
There is an intimate relationship between muscle and bone throughout life. However, how alterations in muscle functions in disease impact bone homeostasis is poorly understood. Amyotrophic lateral sclerosis (ALS) is a neuromuscular disease characterized by progressive muscle atrophy. In this study we analyzed the effects of ALS on bone using the well established G93A transgenic mouse model, which harbors an ALS-causing mutation in the gene encoding superoxide dismutase 1. We found that 4-month-old G93A mice with severe muscle atrophy had dramatically reduced trabecular and cortical bone mass compared with their sex-matched wild type (WT) control littermates. Mechanically, we found that multiple osteoblast properties, such as the formation of osteoprogenitors, activation of Akt and Erk1/2 pathways, and osteoblast differentiation capacity, were severely impaired in primary cultures and bones from G93A relative to WT mice; this could contribute to reduced bone formation in the mutant mice. Conversely, osteoclast formation and bone resorption were strikingly enhanced in primary bone marrow cultures and bones of G93A mice compared with WT mice. Furthermore, sclerostin and RANKL expression in osteocytes embedded in the bone matrix were greatly up-regulated, and β-catenin was down-regulated in osteoblasts from G93A mice when compared with those of WT mice. Interestingly, calvarial bone that does not load and long bones from 2-month-old G93A mice without muscle atrophy displayed no detectable changes in parameters for osteoblast and osteoclast functions. Thus, for the first time to our knowledge, we have demonstrated that ALS causes abnormal bone remodeling and defined the underlying molecular and cellular mechanisms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.