ArticleFoot & ankle international2020
Effect of Metformin on Development of Tendinopathy Due to Mechanical Overloading in an Animal Model.
Article in Foot & ankle international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- The HMGB1/RAGE/β-catenin axis mediates aberrant osteogenic-tenogenic differentiation imbalance of tendon stem/progenitor cells in diabetic tendinopathy.Journal of orthopaedic surgery and research · 2025Article
- Comparative human and porcine skin permeation profiles of novel metformin lotion formulations.Scientific reports · 2025Article
- Metformin Administration Protects Against Deltoid Tendon Damage Through Activation of Notch Signaling.iMeta · 2025Article
- Metformin lotion as a novel approach to prevent tendinopathy induced by mechanical overuse.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
- Article
- Quantifying skin permeation of a novel metformin lotion using modified hydrophilic interaction liquid chromatography.Bioanalysis · 2024Article
- HMGB1 Modulates High Glucose-Induced Erroneous Differentiation of Tendon Stem/Progenitor Cells through RAGE/Stem cells international · 2024Article
- Mitigating Scar Tissue Formation in Tendon Injuries: Targeting HMGB1, AMPK Activation, and Myofibroblast Migration All at Once.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Animal model for tendinopathy.Journal of orthopaedic translation · 2023Review
- The Regulation of the AMPK/mTOR Axis Mitigates Tendon Stem/Progenitor Cell Senescence and Delays Tendon Aging.Stem cell reviews and reports · 2023Article
- Metformin improves tendon degeneration by blocking translocation of HMGB1 and suppressing tendon inflammation and senescence in aging mice.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2023Article
- Mouse Achilles tendons exhibit collagen disorganization but minimal collagen denaturation during cyclic loading to failure.Journal of biomechanics · 2023Article
- Inflammatory mechanisms linking obesity and tendinopathy.Journal of orthopaedic translation · 2021Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
backgroundTendinopathy is a debilitating tendon disorder that affects millions of Americans and costs billions of health care dollars every year. High mobility group box 1 (HMGB1), a known tissue damage signaling molecule, has been identified as a mediator in the development of tendinopathy due to mechanical overloading of tendons in mice. Metformin (Met), a drug approved by the Food and Drug Administration used for the treatment of type 2 diabetes, specifically inhibits HMGB1. This study tested the hypothesis that Met would prevent mechanical overloading-induced tendinopathy in a mouse model of tendinopathy created by intensive treadmill running (ITR).
methodsC57BL/6J mice (female, 3 months old) were equally separated into 4 groups and treated for 24 weeks as follows: group 1 had cage control activities, group 2 received a single intraperitoneal injection of Met (50 mg/kg body weight) daily, group 3 underwent ITR to induce tendinopathy, and group 4 received daily Met injection along with ITR to inhibit HMGB1. Tendinopathic changes were assessed in Achilles tendons of all mice using histology, immunohistochemistry, and enzyme-linked immunosorbent assays.
resultsITR induced HMGB1 release into the tendon matrix and developed characteristics of tendinopathy as evidenced by the expression of macrophage marker CD68, proinflammatory molecules (COX-2, PGE
conclusionsInhibition of HMGB1 by injections of Met prevented tendinopathy development due to mechanical overloading in the Achilles tendon in mice. CLINICAL RELEVANCE: Met may be able to be repurposed as a therapeutic option for preventing the development of tendinopathy in high-risk patients.
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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.