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Although muscle–bone crosstalk is recognized, its shared decline is still not well explained and integrated therapies remain limited. This narrative review argues that a single pathological syndrome is driven by failure of the inflammation-energy metabolism axis. It describes a self-amplifying loop in which inflammaging and dysregulated energy metabolism, including mitochondrial dysfunction and insulin resistance, jointly accelerate synchronized deterioration. The review outlines how chronic inflammation promotes catabolism and resorption, while energy crisis impairs anabolic programs; it also highlights a mechanism where metabolic stress releases DAMPs that further fuel inflammation. It concludes that disrupting this vicious cycle requires systemic, combination, gut microbiota, and exercise-based strategies.",{"@graph":69,"@context":122},[70,84,105],{"@type":71,"itemListElement":72},"BreadcrumbList",[73,77,79,82],{"item":74,"name":75,"@type":76,"position":8},"https://docshare.wps.com","Home","ListItem",{"item":78,"name":9,"@type":76,"position":14},"https://docshare.wps.com/document/",{"item":80,"name":35,"@type":76,"position":81},"https://docshare.wps.com/document/healthcare/",3,{"item":83,"name":65,"@type":76,"position":19},"https://docshare.wps.com/document/the-inflammation-energy-metabolism-axis-a-central-driver-of-sarcopenia-osteoporosis-a-narrative-review/453352/",{"url":83,"name":65,"@type":85,"image":86,"author":91,"headline":65,"publisher":94,"fileFormat":97,"inLanguage":63,"description":67,"dateModified":98,"datePublished":99,"encodingFormat":97,"isAccessibleForFree":100,"interactionStatistic":101},"DigitalDocument",{"url":87,"@type":88,"width":89,"height":90},"https://docshare.wps.com/thumbnails/the-inflammation-energy-metabolism-axis-a-central-driver-of-sarcopenia-osteoporosis-a-narrative-review/453352.png","ImageObject",300,407,{"name":92,"@type":93},"Noah","Person",{"url":74,"name":95,"@type":96},"DocShare","Organization","application/pdf","2026-10-30","2026-09-30",true,{"@type":102,"interactionType":103,"userInteractionCount":39},"InteractionCounter",{"@type":104},"ViewAction",{"@type":106,"mainEntity":107},"FAQPage",[108,114,118],{"name":109,"@type":110,"acceptedAnswer":111},"What does the inflammation-energy metabolism axis explain in sarcopenia-osteoporosis?","Question",{"text":112,"@type":113},"It is presented as the central driver of sarcopenia-osteoporosis, unifying the simultaneous decline of muscle and bone into a single pathological syndrome rather than a coincidental comorbidity.","Answer",{"name":115,"@type":110,"acceptedAnswer":116},"How does chronic low-grade inflammation contribute to muscle and bone deterioration?",{"text":117,"@type":113},"The review links chronic inflammation to muscle catabolism and bone resorption through pathways such as NF-κB and the NLRP3 inflammasome.",{"name":119,"@type":110,"acceptedAnswer":120},"Why is disrupting a vicious cycle emphasized over single-target treatments?",{"text":121,"@type":113},"The described cycle is self-sustaining: inflammation worsens metabolic pathways while metabolic stress releases DAMPs that further amplify inflammation, trapping both tissues in a catabolic state; systemic interventions are therefore needed.","https://schema.org",{"og:url":83,"og:type":124,"og:title":65,"og:site_name":95,"og:description":67},"article",{"robots":126,"canonical":83},"index,follow",{"doc_id":128,"site_id":62},453352,1790977081,{"code":4,"msg":5,"data":131},{"doc_id":128,"user_id":132,"nickname":92,"user_avatar":133,"doc_module":4,"category_id":34,"category_name":35,"doc_title":65,"doc_description":67,"doc_content":134,"file_id":135,"file_url":136,"file_type":137,"file_size":138,"view_count":39,"is_deleted":4,"is_public":8,"is_downloadable":8,"audit_status":8,"page_count":139,"language":140,"language_code":63,"site_id":62,"html_lang":63,"table_of_contents":141,"faqs":142,"seo_title":143,"seo_description":67,"update_tm":144,"read_time":41,"preview_page_count":4},8796095462418,"https://ap-avatar.wpscdn.com/avatar/80000253c1241d02b47?x-image-process=image/resize,m_fixed,w_180,h_180&k=1778826106357471780","Calcified Tissue International (2026) 117:9 [https://doi.org/10.1007/s00223-025-01473-8](https://doi.org/10.1007/s00223-025-01473-8)  \nREVIEW ARTICLE  \nThe Inflammation-Energy Metabolism Axis: A Central Driver of  \nSarcopenia-Osteoporosis: A Narrative Review  \nYifan Jiang1 · Xiaonan Qi2 · Haijian Cui2 · Yingtao Huang1 · Yibo Lv1 · Yu Yang1 · Xiaosheng Yao1,2,3 · Dongxiang Yang4  \nReceived: 9 October 2025 / Accepted: 19 December 2025 © The Author(s) 2026  \nAbstract  \nSarcopenia-osteoporosis, the concomitant loss of muscle and bone mass, is a geriatric comorbidity that significantly increases the risk of falls, fractures, and mortality. Despite the acknowledgment of muscle-bone crosstalk, the underlying mechanism driving their simultaneous decline remains poorly understood, resulting in a lack of effective integrated therapies. This review aims to elucidate the “inflammation-energy metabolism axis” as the central driver of this condition. This review contends that sarcopenia-osteoporosis is not a coincidental comorbidity but a single pathological syndrome driven by the failure of the inflammation-energy metabolism axis. Its pathophysiology is a self-sustaining vicious cycle where chronic low-grade inflammation (inflammaging) and dysregulated energy metabolism (notably mitochondrial dysfunction and insulin resistance) reciprocally amplify each other, leading to synchronous muscle and bone deterioration. The review first details how chronic inflammation, via pathways like NF-κB and the NLRP3 inflammasome, promotes muscle catabolism and bone resorption. Second, it explains how an energy crisis, stemming from mitochondrial damage and insulin resistance, impairs anabolic processes in both tissues. Finally, the underlying cycle is revealed: inflammation disrupts metabolic pathways (e.g., PI3K/AKT/mTOR), while metabolic stress releases DAMPs that further fuel inflammation, trapping the muscle-bone unit in a catabolic state. Understanding this central axis necessitates a paradigm shift from single-target treatments to systemic interventions. Future strategies should focus on disrupting this vicious cycle through combination therapies (e.g., anti-inflammatory and pro-metabolic agents), gut microbiota modulation, and exercise, offering novel approaches to this debilitating comorbidity.  \nKeywords Sarcopenia-osteoporosis · Inflammaging · Energy metabolism · Muscle-bone crosstalk · NF-κB signaling  \nYifan Jiang and Xiaonan Qi have equally contributed to this work.  \n􀀍 Xiaosheng Yao [18102456769@163.com](18102456769@163.com)  \n􀀍 Dongxiang Yang [18102459030@163.com](18102459030@163.com)  \n1 First Clinical School, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China  \n2 Orthopedics and Traumatology, Affiliated Hospital of Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China  \n3 Graduate School, Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China  \n4 Liaoning University of Traditional Chinese Medicine, Shenyang 110847, China  \nIntroduction  \nSarcopenia-Osteoporosis Comorbidity: A New Clinical Issue  \nSarcopenia-osteoporosis refers to a comorbid condition of loss of skeletal muscle mass and function with reduced bone mineral density. It was first proposed by Neil Binkley in the year 2009 [1]and significantly increases the risk of falls, fractures, and death during old age [2] . Studies have shown thatsarcopenic women are 12.9 times more probable to develop osteoporosis, 2.7 times more probable to fracture, and 2.1 times more probable to fall within 12 months compared to non-sarcopenic women [3] . The epidemiology of sarcopenia-osteoporosis worldwide was reported on a meta-analysis and systematic review to be 18.5% in the population aged 46.6 to 93 years [2]. In the United Kingdom, approximately £4 billion annually is spent treating osteoporosis-related  \n1 3  \nfragility fractures [4]; like osteoporosis, sarcopenia puts health systems in billions of dollars every year globally ","cbCaiedVW712VGiW","https://ap.wps.com/l/cbCaiedVW712VGiW","pdf",1240520,12,"English","# Introduction\n## Sarcopenia-Osteoporosis Comorbidity: A New Clinical Issue\n## Muscle-Bone Interaction: from Mechanical Coupling To an Endocrine Network","[{\"question\":\"What does the inflammation-energy metabolism axis explain in sarcopenia-osteoporosis?\",\"answer\":\"It is presented as the central driver of sarcopenia-osteoporosis, unifying the simultaneous decline of muscle and bone into a single pathological syndrome rather than a coincidental comorbidity.\"},{\"question\":\"How does chronic low-grade inflammation contribute to muscle and bone deterioration?\",\"answer\":\"The review links chronic inflammation to muscle catabolism and bone resorption through pathways such as NF-κB and the NLRP3 inflammasome.\"},{\"question\":\"Why is disrupting a vicious cycle emphasized over single-target treatments?\",\"answer\":\"The described cycle is self-sustaining: inflammation worsens metabolic pathways while metabolic stress releases DAMPs that further amplify inflammation, trapping both tissues in a catabolic state; systemic interventions are therefore needed.\"}]","The Inflammation-Energy Metabolism Axis: A Central Driver of Sarcopenia-Osteoporosis - A Narrative Review | PDF",1790738729]