ArticleCell stress & chaperones2015
HSP70 inhibits stress-induced cardiomyocyte apoptosis by competitively binding to FAF1.
Article in Cell stress & chaperones, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.
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Who cites it
13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- Genome-wide association and multi-trait analyses characterize the common genetic architecture of heart failure.Nature communications · 2022Pooled it
- Aerobic exercise in anthracycline-induced cardiotoxicity: a systematic review of current evidence and future directions.American journal of physiology. Heart and circulatory physiology · 2017Pooled it
- Heat Shock Protein 70 Constitutes a Promising Novel Biomarker in Differential Diagnosis between Takotsubo Syndrome and Non-ST-Segment Elevation Myocardial Infarction.Journal of clinical medicine · 2024Article
- Inhibition of circ_0073932 attenuates myocardial ischemia‒reperfusion injury via miR-493-3p/FAF1/JNK.In vitro cellular & developmental biology. Animal · 2024Article
- Expression and Localization of Fas-Associated Factor 1 in Testicular Tissues of Different Ages and Ovaries at Different Reproductive Cycle Phases ofAnimals : an open access journal from MDPI · 2023Article
- Sericin-mediated improvement of dysmorphic cardiac mitochondria from hypercholesterolaemia is associated with maintaining mitochondrial dynamics, energy production, and mitochondrial structure.Pharmaceutical biology · 2022Article
- Hif-1α/Hsf1/Hsp70 signaling pathway regulates redox homeostasis and apoptosis in large yellow croaker (Zoological research · 2021Article
- Cardiac-Specific Deletion of Orai3 Leads to Severe Dilated Cardiomyopathy and Heart Failure in Mice.Journal of the American Heart Association · 2021Article
- Detection of heat shock protein 27, 70, 90 expressions in primary parenchymatous organs of goats after transport stress by real-time PCR and ELISA.Veterinary medicine and science · 2020Article
- Apoptosis in idiopathic inflammatory myopathies with partial invasion; a role for CD8+ cytotoxic T cells?PloS one · 2020Article
- Effects of voluntary exercise on apoptosis and cortisol after chronic restraint stress in mice.Journal of exercise nutrition & biochemistry · 2016Article
- Stress and health Huangshan-style.Cell stress & chaperones · 2016Review
- Glucocorticoids impair oocyte developmental potential by triggering apoptosis of ovarian cells via activating the Fas system.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
11 authors at 1 institution.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stress-induced cardiomyocyte apoptosis plays an important role in the pathogenesis of a variety of cardiovascular diseases. Our early studies showed that HSP70 effectively inhibited apoptosis, but the underlying mechanism remained unclear. Fas-associated factor 1 (FAF1) is a member of the Fas death-inducing signaling complex (Fas-DISC) that acts upstream of caspase-8. We investigated the interactions among FAF1, HSP70, and FAS in stressed cardiomyocytes to elucidate the protective mechanism of HSP70. FAS and caspase-3/8 activity was higher in cardiomyocytes undergoing stress-induced apoptosis in restraint-stressed rats compared with cardiomyocytes in non-stressed rats, which indicated that the Fas signaling pathway was activated after restraint stress. Geranylgeranylacetone (GGA) induced an increase in HSP70 expression, which reduced stress-induced apoptosis. Additionally, overexpression of HSP70 via transfection with the pEGFP-rHSP70 plasmid attenuated norepinephrine (NE)-induced apoptosis. FAF1 expression increased during stress-induced apoptosis, and overexpression of FAF1 exacerbated NE-induced apoptosis. We also found that HSP70 interacted with FAF1. Overexpression of HSP70 inhibited the binding of FAF1 to FAS in H9C2 cells, which indicated that HSP70 suppressed NE-induced apoptosis by competitively binding to FAF1. An N-terminal deletion mutant of HSP70 (HSP70-△N) was unable to interact with FAF1. After HSP70-△N was transfected into H9C2 cells, the cells were unable to attenuate the NE-induced increases in caspase-8 and apoptosis. These results indicate that the 1-120 sequence of HSP70 binds to FAF1, which alters the interactions between FAS and FAF1 and inhibits the activation of the Fas signaling pathway and apoptosis.
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