ArticleShock (Augusta, Ga.)2011
The heat shock paradox and cardiac myocytes: role of heat shock factor.
Article in Shock (Augusta, Ga.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Heat shock factor-1 knockout enhances cholesterol 7α-hydroxylase (CYP7A1) and multidrug transporter (MDR1) gene expressions to attenuate atherosclerosis.Cardiovascular research · 2016Article
- TLR4 mutation and HSP60-induced cell death in adult mouse cardiac myocytes.Cell stress & chaperones · 2015Article
- Comparison of the ventricle muscle proteome between patients with rheumatic heart disease and controls with mitral valve prolapse: HSP 60 may be a specific protein in RHD.BioMed research international · 2014Article
- Heat shock protein 25-enriched plasma transfusion preconditions the heart against doxorubicin-induced dilated cardiomyopathy in mice.The Journal of pharmacology and experimental therapeutics · 2012Article
- Identification of the HSPB4/TLR2/NF-κB axis in macrophage as a therapeutic target for sterile inflammation of the cornea.EMBO molecular medicine · 2012Article
- Celastrol inhibits aminoglycoside-induced ototoxicity via heat shock protein 32.Cell death & disease · 2011Article
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Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
The induction of the heat shock (HS) response is accepted to be a protective response, reducing injury and improving cell survival. However, when inflammation precedes HS, there is an unexpected increase in injury, known as the HS paradox, which is hypothesized to be a mechanism underlying multiorgan dysfunction. We hypothesized that the HS paradox would occur in adult cardiac myocytes and that HS factor (HSF) 1 would contribute to injury. Heat shock at 42°C and TNF (10 ng/mL) were used as the HS and the inflammatory insult, respectively. The combination of TNF followed by HS (TNF/HS) caused the greatest amount of apoptosis in adult rat cardiac myocytes. TNF/HS resulted in an increase in HS protein (HSP) 60, compared with untreated cells, those receiving HS/TNF, or TNF alone. There was no increase in heme oxygenase 1 in any of the groups. Heat shock protein 72 increased in all the groups, with the greatest levels with TNF/HS. Nuclear factor κB activation was greatest with TNF/HS. Pretreatment with a DNA-binding decoy for HSF-1 prevented the increase in HSPs and decreased apoptosis in all groups. However, the increase in iNOS, seen in all treatment groups, was unaffected by the HSF-1-binding decoy. We conclude that the HS paradox occurs in adult cardiac myocytes, that HSP60 is increased as part of the HS paradox, and that HSF-1 activation contributes to injury.
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Registered trials
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