ReviewCurrent osteoporosis reports2025
New Aspects of the Pathophysiology of Diabetic Bone Fragility - Type 2 Diabetes Mellitus as a Disease of Accelerated Aging.
Review in Current osteoporosis reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
purpose of reviewThis 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
findingsMultiple 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. 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.
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Identifiers
What Socratic holds
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 Socratic graph.