ArticleJournal of the American Heart Association2019
Targeting Extracellular Heat Shock Protein 70 Ameliorates Doxorubicin-Induced Heart Failure Through Resolution of Toll-Like Receptor 2-Mediated Myocardial Inflammation.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Extracellular 70 kDa heat shock protein in blood plasma binds insulin and modulates glycaemic control in vivo.Cell stress & chaperones · 2026Article
- Heat shock protein-mediated remodeling of the bone immune microenvironment: mechanisms and precision therapeutic strategies for osteoporosis.Journal of translational medicine · 2026Review
- Functionally diversified Caenorhabditis elegans BiP orthologs control body growth, reproduction, stress resistance, aging, and autophagy.Nature communications · 2025Article
- Aptamers in Drug Delivery Development.Materials today (Kidlington, England) · 2025Article
- Inflammation-Related Factors S100A9 and TLR2 in Cardiomyocyte Hypertrophy.Current medical science · 2025Article
- Programmed Cell Death in Heart Failure: Mechanisms, Impacts, and Therapeutic Prospects.Reviews in cardiovascular medicine · 2025Review
- Cardiac implications of chicken wooden breast myopathy.Frontiers in physiology · 2025Article
- Herbo-Mineral Medicine, Cardiogrit Gold, Exhibits Protective Effects inJournal of toxicology · 2025Article
- Evolution of Theories on Doxorubicin-Induced Late Cardiotoxicity-Role of Topoisomerase.International journal of molecular sciences · 2024Review
- The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death.Cell stress & chaperones · 2024Review
- The role of heat shock proteins in the pathogenesis of heart failure (Review).International journal of molecular medicine · 2023Review
- Zymosan A Improved Doxorubicin-Induced Ventricular Remodeling by Evoking Heightened Cardiac Inflammatory Responses and Healing in Mice.Journal of the American Heart Association · 2023Article
- Extracellular Heat Shock Protein 70 Increases the Glucocorticoid Receptor and Dual-Specificity Phosphatase 1 via Toll-like Receptor 4 and Attenuates Inflammation in Airway Epithelial Cells.International journal of molecular sciences · 2023Article
- Lady's Bedstraw as a Powerful Antioxidant for Attenuation of Doxorubicin-Induced Cardiotoxicity.Antioxidants (Basel, Switzerland) · 2023Article
- Mesaconine alleviates doxorubicin-triggered cardiotoxicity and heart failure by activating PINK1-dependent cardiac mitophagy.Frontiers in pharmacology · 2023Article
- Therapeutic targeting of chronic kidney disease-associated DAMPs differentially contributing to vascular pathology.Frontiers in immunology · 2023Article
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
- Doxorubicin-Induced Cardiotoxicity: An Overview on Pre-clinical Therapeutic Approaches.Cardiovascular toxicology · 2022Review
- The Role of Mitochondrial Quality Control in Anthracycline-Induced Cardiotoxicity: From Bench to Bedside.Oxidative medicine and cellular longevity · 2022Review
- Analysis of Therapeutic Targets of A Novel Peptide Athycaltide-1 in the Treatment of Isoproterenol-Induced Pathological Myocardial Hypertrophy.Cardiovascular therapeutics · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Heart failure (HF) is one of the most significant causes of morbidity and mortality for the cardiovascular risk population. We found previously that extracellular HSP70 (heat shock protein) is an important trigger in cardiac hypertrophy and fibrosis, which are associated with the development of heart dysfunction. However, the potential role of HSP70 in response to HF and whether it could be a target for the therapy of HF remain unknown. Methods and Results An HF mouse model was generated by a single IP injection of doxorubicin at a dose of 15 mg/kg. Ten days later, these mice were treated with an HSP70 neutralizing antibody for 5 times. We observed that doxorubicin treatment increased circulating HSP70 and expression of HSP70 in myocardium and promoted its extracellular release in the heart. Blocking extracellular HSP70 activity by its antibody significantly ameliorated doxorubicin-induced left ventricular dilation and dysfunction, which was accompanied by a significant inhibition of cardiac fibrosis. The cardioprotective effect of the anti-HSP70 antibody was largely attributed to its ability to promote the resolution of myocardial inflammation, as evidenced by its suppression of the toll-like receptor 2-associated signaling cascade and modulation of the intracellular distribution of the p50 and p65 subunits of nuclear factor-κB. Conclusions Extracellular HSP70 serves as a noninfectious inflammatory factor in the development of HF, and blocking extracellular HSP70 activity may provide potential therapeutic benefits for the treatment of HF.
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