ArticleJournal of molecular and cellular cardiology2009
Overexpression of Hsp20 prevents endotoxin-induced myocardial dysfunction and apoptosis via inhibition of NF-kappaB activation.
Article in Journal of molecular and cellular cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- C-terminal extension of HSPB6 in a family with myopathy and cataract.Human molecular genetics · 2026Article
- Pretreatment with interleukin-15 attenuates inflammation and apoptosis by inhibiting NF-κB signaling in sepsis-induced myocardial dysfunction.European journal of histochemistry : EJH · 2024Article
- KLF13 overexpression protects sepsis-induced myocardial injury and LPS-induced inflammation and apoptosis.International journal of experimental pathology · 2023Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Paeoniflorin improves myocardial injury via p38 MAPK/NF-KB p65 inhibition in lipopolysaccharide-induced mouse.Annals of translational medicine · 2021Article
- Traditional Chinese Medicine Targeting Heat Shock Proteins as Therapeutic Strategy for Heart Failure.Frontiers in pharmacology · 2021Review
- Proteomic identification of the proteins related to cigarette smoke-induced cardiac hypertrophy in spontaneously hypertensive rats.Scientific reports · 2020Article
- Fangchinoline attenuates cardiac dysfunction in rats with endotoxemia via the inhibition of ERK1/2 and NF-κB p65 phosphorylation.Annals of translational medicine · 2020Article
- Extracellular vesicles - mediating and delivering cardioprotection in acute myocardial infarction and heart failure.Conditioning medicine · 2020Article
- Reversing Acute Kidney Injury Using Pulsed Focused Ultrasound and MSC Therapy: A Role for HSP-Mediated PI3K/AKT Signaling.Molecular therapy. Methods & clinical development · 2020Article
- Inducible expression of heat shock protein 20 protects airway epithelial cells against oxidative injury involving the Nrf2-NQO-1 pathway.Cell & bioscience · 2020Article
- Attenuation of Experimental Autoimmune Hepatitis in Mice with Bone Mesenchymal Stem Cell-Derived Exosomes Carrying MicroRNA-223-3p.Molecules and cells · 2019Article
- WIPI1 is a conserved mediator of right ventricular failure.JCI insight · 2019Article
- Review
- Alteration of heat shock protein 20 expression in preeclamptic patients and its effect in vascular and coagulation function.Frontiers of medicine · 2018Article
- Quercetin exerts cardiovascular protective effects in LPS-induced dysfunction in vivo by regulating inflammatory cytokine expression, NF-κB phosphorylation, and caspase activity.Molecular and cellular biochemistry · 2018Article
- Circulating Exosomes Isolated from Septic Mice Induce Cardiovascular Hyperpermeability Through Promoting Podosome Cluster Formation.Shock (Augusta, Ga.) · 2018Article
- PDE4-Mediated cAMP Signalling.Journal of cardiovascular development and disease · 2018Review
- HSPB7 prevents cardiac conduction system defect through maintaining intercalated disc integrity.PLoS genetics · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The occurrence of cardiovascular dysfunction in sepsis is associated with a significantly increased mortality rate of 70% to 90% compared with 20% in septic patients without cardiovascular impairment. Thus, rectification or blockade of myocardial depressant factors should partly ameliorate sepsis progression. Heat shock protein 20 (Hsp20) has been shown to enhance myocardial contractile function and protect against doxorubicin-induced cardiotoxicity. To investigate the possible role of Hsp20 in sepsis-mediated cardiac injury, we first examined the expression profiles of five major Hsps in response to lipopolysaccharide (LPS) challenge, and observed that only the expression of Hsp20 was downregulated in LPS-treated myocardium, suggesting that this decrease might be one of the mechanisms contributing to LPS-induced cardiovascular defects. Further studies using loss-of-function and gain-of-function approaches in adult rat cardiomyocytes verified that reduced Hsp20 levels were indeed correlated with the impaired contractile function. In fact, overexpression of Hsp20 significantly enhanced cardiomyocyte contractility upon LPS treatment. Moreover, after administration of LPS (25 microg/g) in vivo, Hsp20 transgenic mice (10-fold overexpression) displayed: 1) an improvement in myocardial function; 2) reduced the degree of cardiac apoptosis; and 3) decreased NF-kappaB activity, accompanied with reduced myocardial cytokines IL-1beta and TNF-alpha production, compared to the LPS-treated non-transgenic littermate controls. Thus, the increases in Hsp20 levels can protect against LPS-induced cardiac apoptosis and dysfunction, associated with inhibition of NF-kappaB activity, suggesting that Hsp20 may be a new therapeutic agent for the treatment of sepsis.
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