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New Aspects of the Pathophysiology of Diabetic Bone Fragility – Type 2 Diabetes Mellitus as a Disease of Accelerated Aging

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Titel: New Aspects of the Pathophysiology of Diabetic Bone Fragility – Type 2 Diabetes Mellitus as a Disease of Accelerated Aging
Autoren: Wölfel, Eva Maria, Kassem, Moustapha
Quelle: Wölfel, E M & Kassem, M 2025, ' New Aspects of the Pathophysiology of Diabetic Bone Fragility – Type 2 Diabetes Mellitus as a Disease of Accelerated Aging ', Current Osteoporosis Reports, vol. 23, no. 1, 45 . https://doi.org/10.1007/s11914-025-00936-z
Verlagsinformationen: 2025.
Publikationsjahr: 2025
Schlagwörter: Aging, Bone quality, Bone fragility, Type 2 diabetes, Cellular senescence
Beschreibung: Purpose of Review: This review summarizes recent findings of the pathophysiology of bone fragility with a particular focus on type 2 diabetes (T2D). It proposes that T2D is a condition of accelerated aging, highlighting mechanisms related to aging as key contributors to bone fragility. Recent Findings: Multiple mechanisms have been proposed to explain the increased fracture risk in individuals with T2D; however, a unified model is still lacking. In this review, we propose that T2D represents a state of accelerated aging, with age-related processes, such as cellular senescence, stem cell exhaustion, enhanced autophagy, intercellular communication, dysbiosis, chronic inflammation, and epigenetic changes including microRNA expression, driving the development of diabetic bone fragility. These mechanisms predominantly impair bone cell function, ultimately compromising bone quality. Summary: The pathophysiology of bone fragility in T2D is discussed within the broader context of aging, emphasizing how fundamental biological mechanisms of the aging process contribute to diabetic bone disease.
Publikationsart: Article
Dateibeschreibung: application/pdf
Sprache: English
DOI: 10.1007/s11914-025-00936-z
Zugangs-URL: https://curis.ku.dk/ws/files/514325710/s11914-025-00936-z.pdf
Dokumentencode: edsair.od......2751..ad3b23ddffceb0f48841616999ab5ac0
Datenbank: OpenAIRE
Beschreibung
Abstract:Purpose of Review: This review summarizes recent findings of the pathophysiology of bone fragility with a particular focus on type 2 diabetes (T2D). It proposes that T2D is a condition of accelerated aging, highlighting mechanisms related to aging as key contributors to bone fragility. Recent Findings: Multiple mechanisms have been proposed to explain the increased fracture risk in individuals with T2D; however, a unified model is still lacking. In this review, we propose that T2D represents a state of accelerated aging, with age-related processes, such as cellular senescence, stem cell exhaustion, enhanced autophagy, intercellular communication, dysbiosis, chronic inflammation, and epigenetic changes including microRNA expression, driving the development of diabetic bone fragility. These mechanisms predominantly impair bone cell function, ultimately compromising bone quality. Summary: The pathophysiology of bone fragility in T2D is discussed within the broader context of aging, emphasizing how fundamental biological mechanisms of the aging process contribute to diabetic bone disease.
DOI:10.1007/s11914-025-00936-z