ArticleAdvances in orthopedics2012
Regulation of hypoxia-induced cell death in human tenocytes.
Article in Advances in orthopedics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed, 34 citations in OpenAlex.
- Cytoprotection as a Unifying Strategy for Hemorrhage and Thrombosis: The Role of BPC 157 and Related Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Tendinopathy of masticatory muscles: a narrative review on the potential pathogenetic mechanism and pain characteristics.Clinical oral investigations · 2026Review
- Tendon, Ligament, and Muscle Injury, Osteotendinous, Myotendinous, and Muscle-to-Bone Junction Therapy Perspectives with Growth Factors and Stable Gastric Pentadecapeptide BPC 157-A Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Signaling pathway networks in frozen shoulder fibrosis: from inflammatory initiation to fibrotic progression.Frontiers in medicine · 2026Review
- Protective and Regenerative Effects of Reconstituted HDL on Human Rotator Cuff Fibroblasts under Hypoxia: An In Vitro Study.Antioxidants (Basel, Switzerland) · 2024Article
- Hypoxia-Inducible Factor and Oxidative Stress in Tendon Degeneration: A Molecular Perspective.Antioxidants (Basel, Switzerland) · 2024Review
- Effect of Aging on Tendon Biology, Biomechanics and Implications for Treatment Approaches.International journal of molecular sciences · 2023Review
- Tendon healing is adversely affected by low-grade inflammation.Journal of orthopaedic surgery and research · 2021Review
- Metabolic Regulation of Tendon Inflammation and Healing Following Injury.Current rheumatology reports · 2021Review
- In Vitro Innovation of Tendon Tissue Engineering Strategies.International journal of molecular sciences · 2020Review
- Adipose-derived stem cells improve tendon repair and prevent ectopic ossification in tendinopathy by inhibiting inflammation and inducing neovascularization in the early stage of tendon healing.Regenerative therapy · 2020Article
- Matrix regeneration proteins in the hypoxia-triggered exosomes of shoulder tenocytes and adipose-derived mesenchymal stem cells.Molecular and cellular biochemistry · 2020Article
- The Effects of Hypoxia-Reoxygenation in Mouse Digital Flexor Tendon-Derived Cells.Oxidative medicine and cellular longevity · 2020Article
- Amplification of Mitochondrial Activity in the Healing Response Following Rotator Cuff Tendon Injury.Scientific reports · 2018Article
- Cellular and molecular maturation in fetal and adult ovine calcaneal tendons.Journal of anatomy · 2015Article
- Transient Exposure to Hypoxic and Anoxic Oxygen Concentrations Promotes Either Osteogenic or Ligamentogenic Characteristics of PDL Cells.BioResearch open access · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Degenerate shoulder tendons display evidence of hypoxia. However tendons are relatively avascular and not considered to have high oxygen requirements and the vulnerability of tendon cells to hypoxia is unclear. Cultured human tenocytes were exposed to hypoxia and the cellular response detected using QPCR, Western blotting, viability, and ELISA assays. We find that tenocytes respond to hypoxia in vitro by activating classical HIF-1α-driven pathways. Total hypoxia caused significant tenocyte apoptosis. Transcription factors typically involved in hypoxic response, HIF-1α and FOXO3A, were upregulated. Hypoxia caused sustained upregulation of several proapoptotic proteins known to mediate hypoxia-induced apoptosis, such as Bnip3 and Nix, but others were unchanged although they were reportedly hypoxia-sensitive in other cell types. Antiapoptotic proteins Bcl2 and Bcl-xL were unchanged by hypoxia. Normal human tenocytes expressed all isoforms of the hypoxia-induced vascular growth factor VEGF except VEGF-D. Hypoxia markedly upregulated VEGF-A mRNA, followed by increased VEGF protein secretion. However treatment with VEGF did not improve tenocyte survival. As a protective strategy for tenocytes at risk of hypoxic death we added prosurvival growth factors insulin or platelet rich plasma (PRP). Both agents strongly protected tenocytes from hypoxia-induced death over 48 h, suggesting possible efficacy in the acute postrupture tendon or integrating graft.
Identifiers
What OpenQuestion 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 OpenQuestion graph.