ArticleCell stress & chaperones2017
Oxidative protein modification alters proteostasis under acute hypobaric hypoxia in skeletal muscles: a comprehensive in vivo study.
Article in Cell stress & chaperones, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- High‑altitude polycythemia: Unveiling the molecular landscape beyond erythropoietin (Review).International journal of molecular medicine · 2026Review
- Unravelling Hypoxia Tolerance: Transcriptomic and Metabolic Insights From Lucinoma capensis in an Oxygen Minimum Zone.Molecular ecology · 2025Article
- Impact of Exposure Duration to High-Altitude Hypoxia on Oxidative Homeostasis in Rat Brain Regions.International journal of molecular sciences · 2025Article
- miR-320-3p regulates apelin and TGF-β/SMAD3 signaling in hypobaric hypoxia exposed rats to induce skeletal muscle atrophy.Journal of physiology and biochemistry · 2025Article
- Hepcidin mediates the disorder of iron homeostasis and mitochondrial function in mice under hypobaric hypoxia exposure.Apoptosis : an international journal on programmed cell death · 2025Article
- Association of altitude and frailty in Chinese older adults: using a cumulative frailty index model.Frontiers in public health · 2024Article
- Hyperbaric oxygen preconditioning for prevention of acute high-altitude diseases: Fact or fiction?Frontiers in physiology · 2023Article
- Mitochondrial Dysfunction as an Underlying Cause of Skeletal Muscle Disorders.International journal of molecular sciences · 2022Review
- Redox status biomarkers in the fast-twitch extensor digitorum longus resulting from the hypoxic exercise.Nagoya journal of medical science · 2022Article
- Oxidative Stress and Diseases Associated with High-Altitude Exposure.Antioxidants (Basel, Switzerland) · 2022Review
- Heat-induced endoplasmic reticulum stress in soleus and gastrocnemius muscles and differential response to UPR pathway in rats.Cell stress & chaperones · 2021Article
- Alterations in the Plasma and Red Blood Cell Properties in Patients with Varicose Vein: A Pilot Study.Cardiology research and practice · 2021Article
- Oxidative Stress, Kinase Activity and Inflammatory Implications in Right Ventricular Hypertrophy and Heart Failure under Hypobaric Hypoxia.International journal of molecular sciences · 2020Review
- Cisplatin-Induced Skeletal Muscle Dysfunction: Mechanisms and Counteracting Therapeutic Strategies.International journal of molecular sciences · 2020Review
- Role of defective CaJournal of cell communication and signaling · 2018Review
- Role of altered proteostasis network in chronic hypobaric hypoxia induced skeletal muscle atrophy.PloS one · 2018Article
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
While numerous maladies are associated with hypobaric hypoxia, muscle protein loss is an important under studied topic. Hence, the present study was designed to investigate the mechanism of muscle protein loss at HH. SD rats were divided into normoxic rats, while remaining rats were exposed to simulated hypoxia equivalent to 282-torr pressure (equal to an altitude of 7620 m, 8% oxygen), at 25 °C for 6, 12, and 24 h. Post-exposure rats were sacrificed and analysis was performed. Ergo, muscle loss-related changes were observed at 12 and 24 h post-HH exposure. An increased reactive oxygen species production and decreased thiol content was observed in HH-exposed rats. This disturbance caused substantial protein oxidative modification in the form of protein carbonyl content and advanced oxidation protein products. The analysis showed increase levels of bityrosine, oxidized tryptophan, lysine conjugate, lysine conjugate with MDA, protein hydroperoxide, and protein-MDA product. These changes were also in agreement with increase in lipid hydroperoxides and MDA content. HSP-70 and HSP-60 were upregulated significantly, and this finding is corroborated with increase in ER stress biomarker, GRP-78. Overloading of cells with misfolded proteins further activated degradative machinery. Consequently, pro-apoptotic signaling cascade, caspase-3, and C/EBP homologous protein were also activated in 24-h HH exposure. Release of tryptophan and tyrosine was also increased with 24-h HH exposure, indicated protein degradation. Elevation in resting intracellular calcium ion, [Ca
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