ArticleGeroScience2025
Cardioprotection and neurobehavioral impact of swimming training in ovariectomized rats.
Article in GeroScience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- miR-203 improves pressure overload-induced heart failure by targeting the IGFBP5/PI3K/AKT axis.Acta pharmacologica Sinica · 2026Article
- Intermittent exercise alleviates MI-induced renal injury in mice via IGF-1.Frontiers in physiology · 2025Article
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Authors and funding
14 authors.
Funding
Abstract
Cardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause, CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due to the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS, improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, the aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish the IGF-1 effect, suggesting that directly or indirectly GPER is part of the IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in the heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade.
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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 Socratic graph.