ArticleCellular and molecular life sciences : CMLS2024
Brown fat-specific mitoribosomal function is crucial for preventing cold exposure-induced bone loss.
Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Marrow fatty acids in osteoporosis: metabolic insights, emerging therapeutic targets.Journal of bone and mineral metabolism · 2026Review
- Cold exposure and human metabolism: A heterogeneous response across tissues and organs.Temperature (Austin, Tex.) · 2026Review
- Immune reprogramming in the bone marrow microenvironment: a new perspective on the bone immune microenvironment of postmenopausal osteoporosis.Frontiers in immunology · 2026Review
- Developing an IPF Prognostic Model and Screening for Key Genes Based on Cold Exposure-Related Genes Using Bioinformatics Approaches.Biomedicines · 2025Article
- Osteocytes function as biomechanical signaling hubs bridging mechanical stress sensing and systemic adaptation.Frontiers in physiology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
This study examines the interplay between ambient temperature, brown adipose tissue (BAT) function, and bone metabolism, emphasizing the effects of cold exposure and BAT mitochondrial activity on bone health. Utilizing ovariectomized (OVX) mice to model primary osteoporosis and BAT-specific mitochondrial dysfunction (BKO) mice, we evaluated the impact of housing temperature on bone density, immune modulation in bone marrow, and the protective role of BAT against bone loss. Cold exposure was found to universally reduce bone mass, enhance osteoclastogenesis, and alter bone marrow T-cell populations, implicating the immune system in bone remodeling under cold stress. The thermogenic function of BAT, driven by mitochondrial oxidative phosphorylation, was crucial in protecting against bone loss. Impaired BAT function, through surgical removal or mitochondrial dysfunction, exacerbated bone loss in cold environments, highlighting BAT's metabolic role in maintaining bone health. Furthermore, cold-induced changes in BAT function led to systemic metabolic shifts, including elevated long-chain fatty acids, which influenced osteoclast differentiation and activity. These findings suggest a systemic mechanism connecting environmental temperature and BAT metabolism with bone physiology, providing new insights into the metabolic and environmental determinants of bone health. Future research could lead to novel bone disease therapies targeting these pathways.
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Registered trials
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