ReviewOpen life sciences2023
Inflammation-related signaling pathways in tendinopathy.
Review in Open life sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- Application of 18Journal of enzyme inhibition and medicinal chemistry · 2026Article
- Article
- A biomimetic hybrid membrane vesicle nanoplatform attenuates tendinopathy through neuroinflammation modulation and tendon regeneration.Cell reports. Medicine · 2026Article
- Engineered Extracellular Vesicles for Treatment of Inflammatory Diseases.Molecular biotechnology · 2026Review
- Allogeneic Platelet-Rich Gel Supernatant Reprograms the Cytokine and Growth Factor Microenvironment in an Equine In Vitro Inflammatory Tendon System.International journal of molecular sciences · 2026Article
- Ankle Joint Biomechanics in Recreational Runners with Resolved and Incident Plantar Fasciitis: A One-Year Prospective 4HAIE Cohort Study.Scandinavian journal of medicine & science in sports · 2026Article
- The Role of Phagocytic Cells in the Achilles Tendon.International journal of molecular sciences · 2026Review
- Changes in gut microbiota and plasma metabolites in patients with symptomatic degenerative rotator cuff tendinopathy.Frontiers in microbiology · 2026Article
- Amniotic Membrane and Stem Cells Can Improve the Immunohistochemical Profile of Achilles Tendons in Injured Rats.Biomedicines · 2025Article
- Regenerative biologics modulating inflammation and promoting tenogenesis in equine superficial digital flexor tendonitis: from molecular pathways to clinical translation.Irish veterinary journal · 2025Review
- Long-Term Preoperative Nonsteroidal Anti-inflammatory Drug Use Does Not Impact Revision Rate After Repair of Rotator Cuff, Achilles, Distal Biceps, or Quadriceps Tendon.Arthroscopy, sports medicine, and rehabilitation · 2025Article
- Regenerative potential of immune cells after traumatic muscle injury.Frontiers in immunology · 2025Review
- Inducing In Situ MBiomaterials research · 2025Article
- Modulation of EGR1 Expression by Hyperglycemia in Swine Rotator Cuff Tendons.Journal of orthopaedics and sports medicine · 2025Article
- Myeloid Cells and Sensory Nerves Mediate Peritendinous Adhesion Formation via Prostaglandin E2.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Assessing Bioprinted Functionalized Grafts for Biological Tendon Augmentation In Vitro.International journal of molecular sciences · 2024Article
- Treatment of Tendon Injuries in the Servicemember Population across the Spectrum of Pathology: From Exosomes to Bioinductive Scaffolds.Bioengineering (Basel, Switzerland) · 2024Review
- Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tendon is a connective tissue that produces movement by transmitting the force produced by muscle contraction to the bones. Most tendinopathy is caused by prolonged overloading of the tendon, leading to degenerative disease of the tendon. When overloaded, the oxygen demand of tenocytes increases, and the tendon structure is special and lacks blood supply, which makes it easier to form an oxygen-deficient environment in tenocytes. The production of reactive oxygen species due to hypoxia causes elevation of inflammatory markers in the tendon, including PGE2, IL-1β, and TNF-α. In the process of tendon healing, inflammation is also a necessary stage. The inflammatory environment formed by cytokines and various immune cells play an important role in the clearance of necrotic material, the proliferation of tenocytes, and the production of collagen fibers. However, excessive inflammation can lead to tendon adhesions and hinder tendon healing. Some important and diverse biological functions of the body originate from intercellular signal transduction, among which cytokine mediation is an important way of signal transduction. In particular, NF-κB, NLRP3, p38/MAPK, and signal transducer and activator of transcription 3, four common signaling pathways in tendinopathy inflammatory response, play a crucial role in the regulation and transcription of inflammatory factors. Therefore, summarizing the specific mechanisms of inflammatory signaling pathways in tendinopathy is of great significance for an in-depth understanding of the inflammatory response process and exploring how to inhibit the harmful part of the inflammatory response and promote the beneficial part to improve the healing effect of the tendon.
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Registered trials
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