ArticleCell stress & chaperones2022
HSP70 protects H9C2 cells from hypoxia and reoxygenation injury through STIM1/IP3R.
Article in Cell stress & chaperones, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Integrated Bioinformatics and Experimental Validation of Post-Translational Modification-Related Biomarkers in Myocardial Ischemia-Reperfusion Injury.Journal of cardiovascular translational research · 2026Article
- Hspa1b attenuates hypoxia/reoxygenation-induced cardiomyocyte injury through dual suppression of P53-driven apoptotic and ferroptotic pathways.Cell stress & chaperones · 2026Article
- Host stress proteins shape hemorrhagic shock via gut microbiota: evidence from Mendelian randomization and animal models.Journal of translational medicine · 2025Article
- Experience-mediated transcriptional memory correlates with hypoxia resistance in the nervous system of the sea hareAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2025Article
- Verbascoside attenuates myocardial ischemia/reperfusion-induced ferroptosis following heterotopic heart transplantation via modulating GDF15/GPX4/SLC7A11 pathway.Scientific reports · 2025Article
- Protective Effects of Rat Bone Marrow Mesenchymal Stem Cells-Derived Fusogenic Plasma Membrane Vesicles Containing VSVG Protein Mediated Mitochondrial Transfer on Myocardial Injury In Vitro.FASEB bioAdvances · 2025Article
- Advances in Chinese herbal medicine in modulating mitochondria to treat myocardial ischemia-reperfusion injury: a narrative review.Cardiovascular diagnosis and therapy · 2025Review
- Mitochondria-Associated Organelle Crosstalk in Myocardial Ischemia/Reperfusion Injury.Journal of cardiovascular translational research · 2024Review
- HSP105 inhibition downregulates store-operated calcium entry and promotes acute UVB-induced tight junction disruption.PloS one · 2024Article
- Tilianin suppresses NLRP3 inflammasome activation in myocardial ischemia/reperfusion injury via inhibition of TLR4/NF-κB and NEK7/NLRP3.Frontiers in pharmacology · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypoxia/reoxygenation (H/R) is used as an in vivo model of ischemia/reperfusion injury, and myocardial ischemia can lead to heart disease. Calcium overload is an important factor in myocardial ischemia-reperfusion injury and can lead to apoptosis of myocardial cells. Therefore, it is of great clinical importance to find ways to regulate calcium overload and reduce apoptosis of myocardial cells, and thus alleviate myocardial ischemia-reperfusion injury. There is evidence that heat shock protein 70 (HSP70) has a protective effect on the myocardium, but the exact mechanism of this effect is not completely understood. Stromal interaction molecule 1 and inositol 1,4,5-triphosphate receptor (STIM/1IP3R) play an important role in myocardial ischemia-reperfusion injury. Therefore, this study aimed to investigate whether HSP70 plays an anti-apoptotic role in H9C2 cardiomyocytes by regulating the calcium overload pathway through STIM1/IP3R. Rat H9C2 cells were subjected to transient oxygen and glucose deprivation (incubated in glucose-free medium and hypoxia for 6 h) followed by re-exposure to glucose and reoxygenation (incubated in high glucose medium and reoxygenation for 4 h) to simulate myocardial ischemia reperfusion-induced cell injury. H9C2 cell viability was significantly decreased, and lactate dehydrogenase (LDH) release and apoptosis were significantly increased after oxygen and glucose deprivation. Transfection of HSP70 into H9C2 cells could reduce the corresponding effect, increase cell viability and anti-apoptotic signal pathway, and reduce the apoptotic rate and pro-apoptotic signal pathway. After hypoxia and reoxygenation, the expression of STIM1/IP3R and intracellular calcium concentration of HSP70-overexpressed H9C2 cells were significantly lower than those of hypoxia cells. Similarly, direct silencing of STIM1 by siRNA significantly increased cell viability and expression of anti-apoptotic protein Bcl-2 and decreased apoptosis rate and expression of pro-apoptotic protein BAX. These data are consistent with HSP70 overexpression. These results suggest that HSP70 abrogates intracellular calcium overload by inhibiting upregulation of STIM1/IP3R expression, thus reducing apoptosis in H9C2 cells and playing a protective role in cardiomyocytes.
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