ArticleJournal of cellular and molecular medicine2020
Pioglitazone attenuates advanced glycation end products-induced apoptosis and calcification by modulating autophagy in tendon-derived stem cells.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Effects of advanced glycation end products (AGEs) on the differentiation potential of primary stem cells: a systematic review.Stem cell research & therapy · 2023Pooled it
- Shared mechanisms of musculoskeletal dysfunction in type 2 diabetes mellitus: Insights into future therapeutic directions (Review).International journal of molecular medicine · 2026Review
- Serum Advanced Glycation End Products as Drivers of Poor Tendon Outcomes in Diabetes? An Emerging Hypothesis and Narrative Review.Endocrinology, diabetes & metabolism · 2026Review
- 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
- Pioglitazone reduces hepatic α-1 antitrypsin accumulation through autophagy and AMPK activation in α-1 antitrypsin-deficient mice.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Tendon Aging: A Silent Enemy Revealed Strategies for Effective Treatment.Aging medicine (Milton (N.S.W)) · 2025Review
- Erroneous Differentiation of Tendon Stem/Progenitor Cells in the Pathogenesis of Tendinopathy: Current Evidence and Future Perspectives.Stem cell reviews and reports · 2025Review
- Tendon Tissue Engineering: Pathophysiological Mechanism and Bioengineering Therapy of Tendinopathy.International journal of nanomedicine · 2025Review
- How to enhance MSCs therapeutic properties? An insight on potentiation methods.Stem cell research & therapy · 2024Review
- Advanced glycation end products impair the repair of injured tendon: a study in rats.BMC musculoskeletal disorders · 2024Article
- Role of β-cell autophagy in β-cell physiology and the development of diabetes.Journal of diabetes investigation · 2024Review
- 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
- The impact of diabetes mellitus on tendon pathology: a review.Frontiers in pharmacology · 2024Review
- Pristimerin suppresses AIM2 inflammasome by modulating AIM2-PYCARD/ASC stability via selective autophagy to alleviate tendinopathy.Autophagy · 2024Article
- Effect of Diabetes on Tendon Structure and Function: Not Limited to Collagen Crosslinking.Journal of diabetes science and technology · 2023Article
- Research progress on the relationship between autophagy and chronic complications of diabetes.Frontiers in physiology · 2022Review
- Editorial: Autophagy in diseases-From basic to clinic.Frontiers in physiology · 2022Article
- Human Achilles tendon mechanical behavior is more strongly related to collagen disorganization than advanced glycation end-products content.Scientific reports · 2021Article
- Characterization of Tendon-Derived Stem Cells and Rescue Tendon Injury.Stem cell reviews and reports · 2021Review
- Advanced glycation end productions and tendon stem/progenitor cells in pathogenesis of diabetic tendinopathy.World journal of stem cells · 2021Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetes mellitus (DM) is one of the prominent risk factors for pathological development and progression of tendinopathy. One feature of DM-related changes in tendinopathy is accumulation of advanced glycation end products (AGEs) in affected tendons. Pioglitazone (Pio), a peroxisome proliferator-activated receptor γ agonist, performs a protective effect against AGEs. The present study aimed to investigate the pathogenetic role of AGEs on tendon-derived stem cells (TDSCs) and to determine the effect of Pio on AGEs-induced TDSC dysfunctions. Results indicated that AGEs induced TDSC apoptosis as well as compensatory activation of autophagy. Pharmacologic activation/inhibition of autophagy leaded to alleviate/exacerbate apoptosis induced by AGEs. We further confirmed the effect of Pio on autophagy, which ameliorated apoptosis and abnormal calcification caused by AGEs both in vitro and in vivo. Thus, we suggest that Pio ameliorates the dysfunctions of TDSCs against AGEs by promoting autophagy, and we also reveal that Pio is a potential pharmacological choice for tendinopathy.
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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 OpenQuestion graph.