ArticleOpen life sciences2025
Clusterin activates the heat shock response via the PI3K/Akt pathway to protect cardiomyocytes from high-temperature-induced apoptosis.
Article in Open life sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
1 citing paper in PubMed.
- [Disease burden and risk factors of myocarditis among children and adolescents aged 0-19 years in China from 1990 to 2021 and projection of future disease burden trends].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026Article
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Authors and funding
4 authors.
Funding
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Abstract
High temperature (HT) is a common symptom of infectious myocarditis. This study investigates the effects of HT on the heat shock response (HSR) and apoptosis in cardiomyocytes, with the aim of providing insights into potential treatment strategies for myocarditis. Rat cardiomyocytes (H9c2 cells) were exposed to 42°C for 1 h, followed by a return to 37°C to simulate high fever conditions. The cells were divided into seven groups: control, oe-NC, oe-CLU, HT, HT + oe-NC, HT + oe-CLU, and HT + oe-CLU + LY294002 (PI3K inhibitor). Protein levels of HSP70, HSP90, Bax, Bcl2, CLU, p-PI3K, and p-Akt were measured by Western blot, while mRNA expression of HSP70, HSP90, Bax, Bcl2, and CLU was assessed via reverse transcription quantitative polymerase chain reaction. Cell proliferation (cell counting kit-8 assay), apoptosis (flow cytometry), and reactive oxygen species (ROS) levels (MitoSOX assay) were also evaluated. HT exposure led to decreased cell proliferation, increased apoptosis, and elevated ROS levels (
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