ArticleCell stress & chaperones2007
Hsp70 may protect cardiomyocytes from stress-induced injury by inhibiting Fas-mediated apoptosis.
Article in Cell stress & chaperones, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 64 citations in OpenAlex.
- Review
- Acupuncture-induced HSP70 upregulation in neuroprotection: mitochondrial and anti-apoptotic mechanisms.American journal of translational research · 2026Review
- Effects of Saccharomyces Cerevisiae Cultures on Performance and Immune Performance of Dairy Cows During Heat Stress.Frontiers in veterinary science · 2022Article
- Sevoflurane Postconditioning Reduces Hypoxia/Reoxygenation Injury in Cardiomyocytes via Upregulation of Heat Shock Protein 70.Journal of microbiology and biotechnology · 2021Article
- Heat Shock Proteins: Potential Modulators and Candidate Biomarkers of Peripartum Cardiomyopathy.Frontiers in cardiovascular medicine · 2021Review
- Combination of exercise training and L-arginine reverses aging process through suppression of oxidative stress, inflammation, and apoptosis in the rat heart.Pflugers Archiv : European journal of physiology · 2020Article
- Effect of sympathetic autonomic stress from the cold pressor test on left ventricular function in young healthy adults.Physiological reports · 2019Article
- Heart irradiation reduces microvascular density and accumulation of HSPA1 in mice.Strahlentherapie und Onkologie : Organ der Deutschen Rontgengesellschaft ... [et al] · 2018Article
- Article
- Cardiac Electrical and Structural Changes During Bacterial Infection: An Instructive Model to Study Cardiac Dysfunction in Sepsis.Journal of the American Heart Association · 2016Article
- Emotional Stress and Cardiovascular Complications in Animal Models: A Review of the Influence of Stress Type.Frontiers in physiology · 2016Review
- HSP70 inhibits stress-induced cardiomyocyte apoptosis by competitively binding to FAF1.Cell stress & chaperones · 2015Article
- Susceptibility of murine induced pluripotent stem cell-derived cardiomyocytes to hypoxia and nutrient deprivation.Stem cell research & therapy · 2015Article
- Tyrosol prevents ischemia/reperfusion-induced cardiac injury in H9c2 cells: involvement of ROS, Hsp70, JNK and ERK, and apoptosis.Molecules (Basel, Switzerland) · 2015Article
- Effects of HIP in protection of HSP70 for stress-induced cardiomyocytes injury and its glucorticoid receptor pathway.Cell stress & chaperones · 2014Article
- Structural and functional analysis of novel human cytochrome C targets in apoptosis.Molecular & cellular proteomics : MCP · 2014Article
- Article
- A protective Hsp70-TLR4 pathway in lethal oxidant lung injury.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Heat shock protein 72 enhances autophagy as a protective mechanism in lipopolysaccharide-induced peritonitis in rats.The American journal of pathology · 2011Article
- Heat shock protein expression and change of cytochrome c oxidase activity: presence of two phylogenic old systems to protect tissues in ischemia and reperfusion.Journal of bioenergetics and biomembranes · 2011Review
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of Hsp70 is an endogenous mechanism by which living cells adapt to stress and the protection of Hsp70 may interfere with the apoptotic machinery in a variety of ways. Here, we observed the change of Hsp70 expression in rat myocardium under stress and explored the protective effect of Hsp70 on the Fas-mediated pathway to cardiomyocyte apoptosis. The results showed that restraint stress led to cardiac dysfunction and structural damage of the myocardium, as well as activation of the Fas pathway. A similar increase in the Fas expression level, caspase-8/3 activity, and the apoptotic rate of the cardiomyocyte also were found, which indicated that Fas-mediated apoptosis of cardiomyocytes might be one of the mechanisms of cardiomyocyte injury induced by stress. Changes in Hsp70 levels and distribution occurred during the stress process, which correlated with the severity of myocardium injury. Heat preconditioning induced the upregulation of Hsp70 synthesis, which in turn may have mitigated subsequent restraint stress-induced damage, including electrocardiography (ECG) abnormality, myocardium damage, and cell death. Moreover, Hsp70 overexpression induced by heat preconditioning had no effect on Fas expression in the cardiomyocyte, but could inhibit activation of caspase-8/3 induced by the Fas signaling pathway and, as a result, prevent cell apoptosis. These results suggest that Hsp70 is capable of protecting the cardiomyocyte from stress-induced injury by inhibiting Fas-mediated apoptosis, and Hsp70 could be considered a target in future drugs to prevent cardiovascular injury caused by stress.
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