ArticleHeart and vessels2015
The protective effect of heat shock protein 70 (Hsp70) in atrial fibrillation in various cardiomyopathy conditions.
Article in Heart and vessels, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Review
- Alarmins as a Possible Target of Future Therapies for Atrial Fibrillation.International journal of molecular sciences · 2022Review
- Untying the knot: protein quality control in inherited cardiomyopathies.Pflugers Archiv : European journal of physiology · 2019Review
- Immunopathogenesis and biomarkers of recurrent atrial fibrillation following ablation therapy in patients with preexisting atrial fibrillation.Expert review of cardiovascular therapy · 2019Review
- Effects of a Proteasome Inhibitor on Cardiomyocytes in a Pressure-Overload Hypertrophy Rat Model: An Animal Study.The Korean journal of thoracic and cardiovascular surgery · 2017Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heat shock proteins (Hsp) protect myocardial cells from acute stress such as atrial fibrillation (AF) and also from the chronic stress. It is not understood that Hsp70 can prevent AF under cardiomyopathy (CM) conditions. Therefore, we hypothesized that Hsp70 might beneficially influence on the occurrence of AF in CM conditions. We purposed to investigate the correlation between Hsp70 and the AF inducibility in various CM conditions that are unclear. We constructed four different animal models using Sprague-Dawley rats: an ischemic CM group (n = 12), a non-ischemic dilated CM group (n = 12), a pressure-overload hypertrophic CM group (n = 12), and a sham group (CON, n = 12). After 4-6 weeks of intervention animals, AF was induced acutely prior to hemodynamic studies. Hemodynamic data using the Langendorff technique and histologic evaluation were conducted sequentially in all animal groups. Afterwards, levels of Hsp70 were measured from atrial tissues by real-time polymerase chain reaction study. The hemodynamic data and histologic studies proved that each animal model was suitable to this study protocol. All CM groups showed that Hsp70 was elevated significantly compared to the control groups (P < 0.005). Among these CM groups, the TAC group revealed lower Hsp70 levels and higher induction rates of atrial fibrillation than the other groups (P < 0.005). The level of Hsp70 was elevated in all the CM models and it was negatively correlated with AF induction rate in sham group. However, we could not find correlation between Hsp70 and AF among the CM models.
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