ArticleScientific reports2019
Advanced Glycation End-Products Suppress Mitochondrial Function and Proliferative Capacity of Achilles Tendon-Derived Fibroblasts.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Serum Advanced Glycation End Products as Drivers of Poor Tendon Outcomes in Diabetes? An Emerging Hypothesis and Narrative Review.Endocrinology, diabetes & metabolism · 2026Review
- An Angiotensin II Receptor Blocker Suppresses Glucose-Induced Oxidative Stress in Human Rotator Cuff-Derived Cells.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Synaptic mitochondria in aging and neurodegenerative diseases: Functional decline and vulnerability.Neural regeneration research · 2026Article
- Nutritional Interventions to Optimize Orthobiologic Therapy Quality in Type 2 Diabetes Mellitus: Molecular Mechanisms and Clinical Framework: A Narrative Review.International journal of molecular sciences · 2026Review
- Achilles tenocytes from diabetic and non diabetic donors exposed to hyperglycemia respond differentially to inflammatory stimuli and stretch.Journal of anatomy · 2026Article
- Beyond local injury: pathogenic roles of metabolic, endocrine, and aging-associated systemic factors in tendinopathy and novel therapeutic strategies.Journal of orthopaedic surgery and research · 2026Review
- Role of Advanced Glycation End Products and Mitohormesis in Cancer Development and Progression.Antioxidants (Basel, Switzerland) · 2025Review
- Regulating inflammation microenvironment and tenogenic differentiation as sequential therapy promotes tendon healing in diabetic rats.Journal of orthopaedic translation · 2025Article
- Elevated glycated haemoglobin affects Achilles tendon properties and walking capacity in healthy people without a diagnosis of diabetes.Scientific reports · 2025Article
- AMP-activated protein kinase (AMPK) is essential for tendon homeostasis and prevents premature senescence and ectopic calcification.bioRxiv : the preprint server for biology · 2025Article
- Tendon Tissue Engineering: Pathophysiological Mechanism and Bioengineering Therapy of Tendinopathy.International journal of nanomedicine · 2025Review
- Advanced glycation end products promote ROS production via PKC/p47 phox axis in skeletal muscle cells.The journal of physiological sciences : JPS · 2024Article
- Advanced glycation end products impair the repair of injured tendon: a study in rats.BMC musculoskeletal disorders · 2024Article
- Localization of advanced glycation end-products and their receptor in tendinopathic lesions.Histology and histopathology · 2024Article
- Pioglitazone Antagonized the Effects of Advanced Glycation End Products on Achilles Tendon Healing and Improved the Recovery of Tendon Biomechanical Properties.Cellular and molecular bioengineering · 2024Article
- Evaluation of suitable reference genes for qPCR normalisation of gene expression in a Achilles tendon injury model.PloS one · 2024Article
- Combined therapeutic strategy based on blocking the deleterious effects of AGEs for accelerating diabetic wound healing.Regenerative biomaterials · 2024Article
- Non-Genomic Hallmarks of Aging-The Review.International journal of molecular sciences · 2023Review
- Effect of Aging on Tendon Biology, Biomechanics and Implications for Treatment Approaches.International journal of molecular sciences · 2023Review
- Sound touch elastography of Achilles tendons in patients with type 2 diabetes mellitus versus healthy adults.Diabetology & metabolic syndrome · 2023Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Debilitating cases of tendon pain and degeneration affect the majority of diabetic individuals. The high rate of tendon degeneration persists even when glucose levels are well controlled, suggesting that other mechanisms may drive tendon degeneration in diabetic patients. The purpose of this study was to investigate the impact of advanced glycation end-products on tendon fibroblasts to further our mechanistic understanding of the development and progression of diabetic tendinopathy. We proposed that advanced glycation end-products would induce limitations to mitochondrial function and proliferative capacity in tendon-derived fibroblasts, restricting their ability to maintain biosynthesis of tendon extracellular matrix. Using an in-vitro cell culture system, rat Achilles tendon fibroblasts were treated with glycolaldehyde-derived advanced glycation end-products (0, 50, 100, and 200 μg/ml) for 48 hours in normal glucose (5.5 mM) and high glucose (25 mM) conditions. We demonstrate that tendon fibroblasts treated with advanced glycation end-products display reduced ATP production, electron transport efficiency, and proliferative capacity. These impairments were coupled with alterations in mitochondrial DNA content and expression of genes associated with extracellular matrix remodeling, mitochondrial energy metabolism, and apoptosis. Our findings suggest that advanced glycation end-products disrupt tendon fibroblast homeostasis and may be involved in the development and progression of diabetic tendinopathy.
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Registered trials
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