ArticleFrontiers in pharmacology2020
Heat Shock Protein 22 Attenuates Doxorubicin-Induced Cardiotoxicity
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Shikimic acid protects against doxorubicin-induced cardiotoxicity in rats.Scientific reports · 2025Article
- Heat shock protein 22: A new direction for cardiovascular disease (Review).Molecular medicine reports · 2025Review
- Imidacloprid exposure in rats induces cardiac inflammatory response through activating TLR4/NF-κB/NLRP3 and JAK/STAT signaling pathways: focus on the berberine-loaded nanoliposomes.Frontiers in toxicology · 2025Article
- CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling.Cardiovascular drugs and therapy · 2024Article
- Neutrophil Biomarkers Can Predict Cardiotoxicity of Anthracyclines in Breast Cancer.International journal of molecular sciences · 2024Article
- Role of Oxidative Stress and Inflammation in Doxorubicin-Induced Cardiotoxicity: A Brief Account.International journal of molecular sciences · 2024Review
- A review of chemotherapeutic drugs-induced arrhythmia and potential intervention with traditional Chinese medicines.Frontiers in pharmacology · 2024Review
- α-Bisabolol, a Dietary Sesquiterpene, Attenuates Doxorubicin-Induced Acute Cardiotoxicity in Rats by Inhibiting Cellular Signaling Pathways, Nrf2/Keap-1/HO-1, Akt/mTOR/GSK-3β, NF-κB/p38/MAPK, and NLRP3 Inflammasomes Regulating Oxidative Stress and Inflammatory Cascades.International journal of molecular sciences · 2023Article
- Nrf2: a dark horse in doxorubicin-induced cardiotoxicity.Cell death discovery · 2023Review
- Toll-like Receptor 4 Inflammatory Perspective on Doxorubicin-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2023Review
- Article
- Tubeimoside I Ameliorates Doxorubicin-Induced Cardiotoxicity by Upregulating SIRT3.Oxidative medicine and cellular longevity · 2023Article
- The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument.Inflammopharmacology · 2022Article
- Selenium Attenuates Doxorubicin-Induced Cardiotoxicity Through Nrf2-NLRP3 Pathway.Biological trace element research · 2022Article
- Combination ofFrontiers in pharmacology · 2022Article
- Hsp22 ameliorates lipopolysaccharide-induced myocardial injury by inhibiting inflammation, oxidative stress, and apoptosis.Bioengineered · 2021Article
- Systematic insight into the active constituents and mechanism of Guiqi Baizhu for the treatment of gastric cancer.Cancer science · 2021Article
- NLRP3 Inflammasome: A Promising Therapeutic Target for Drug-Induced Toxicity.Frontiers in cell and developmental biology · 2021Review
- Phosphorylation Modifications Regulating Cardiac Protein Quality Control Mechanisms.Frontiers in physiology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe antitumor effect of doxorubicin (DOX) is limited by its acute and chronic toxicity to the heart, which causes heart injury. Heat shock protein 22 (Hsp22) is a protein proved to exert anti-apoptosis and anti-inflammatory effects in other diseases and physical conditions. In this study, we aim to explore whether Hsp22 could exert a protective role during cardiac injury in response to DOX.
methodsThe overexpression of Hsp22 was mediated
resultsAn increase in the expression level of Hsp22 was observed in DOX-treated heart tissue. Furthermore, cardiac-specific overexpression of Hsp22 showed reduced cardiac dysfunction, decrease in inflammatory response, and reduction in cell apoptosis in injury heart and cardiomyocytes induced by DOX
conclusionIn summary, Hsp22 overexpression in the heart could suppress cardiac injury in response to DOX treatment through blocking TLR4/NLRP3 activation. Hsp22 may become a new therapeutic method for treating cardiac injury induced by DOX in cancer patients.
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