ArticleJournal of cellular and molecular medicine2020
TLR9 deficiency alleviates doxorubicin-induced cardiotoxicity via the regulation of autophagy.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 41 citations in OpenAlex.
- The mitochondrial protease, LonP1, is a potential cardioprotective target for attenuating doxorubicin-induced cardiomyocyte death.Journal of translational medicine · 2026Article
- Mechanisms and the Role of p38 MAPK Signaling in Doxorubicin-Induced Cardiotoxicity: A Review.International journal of general medicine · 2026Review
- Cationic microparticles inhibit local sterile inflammation in tissue injuries.Regenerative biomaterials · 2026Article
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.Autophagy reports · 2025Review
- Triad3A-Mediated K48-Linked ubiquitination and degradation of TLR9 impairs mitochondrial bioenergetics and exacerbates diabetic cardiomyopathy.Journal of advanced research · 2024Article
- FUNDC1 alleviates doxorubicin-induced cardiotoxicity by restoring mitochondrial-endoplasmic reticulum contacts and blocked autophagic flux.Theranostics · 2024Article
- RGS7 balances acetylation/de-acetylation of p65 to control chemotherapy-dependent cardiac inflammation.Cellular and molecular life sciences : CMLS · 2023Article
- Mitochondrial Dysfunction Associated with mtDNA in Metabolic Syndrome and Obesity.International journal of molecular sciences · 2023Review
- BNIP3-mediated autophagy via the mTOR/ULK1 pathway induces primordial follicle loss after ovarian tissue transplantation.Journal of assisted reproduction and genetics · 2023Article
- The Innate Immune System in Cardiovascular Diseases and Its Role in Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2022Review
- Bone morphogenetic protein 10 alleviates doxorubicin-induced cardiac injury via signal transducer and activator of transcription 3 signaling pathway.Bioengineered · 2022Article
- The Role of Flavonoids as a Cardioprotective Strategy against Doxorubicin-Induced Cardiotoxicity: A Review.Molecules (Basel, Switzerland) · 2022Review
- NEU1 Regulates Mitochondrial Energy Metabolism and Oxidative Stress Post-myocardial Infarction in MiceFrontiers in cardiovascular medicine · 2022Article
- MicroRNA-181a-5p Promotes Osteosarcoma Progression via PTEN/AKT Pathway.Analytical cellular pathology (Amsterdam) · 2022Article
- Peptide Szeto‑Schiller 31 ameliorates doxorubicin‑induced cardiotoxicity by inhibiting the activation of the p38 MAPK signaling pathway.International journal of molecular medicine · 2021Article
- MicroRNA-223-3p Protect Against Radiation-Induced Cardiac Toxicity by Alleviating Myocardial Oxidative Stress and Programmed Cell DeathFrontiers in cell and developmental biology · 2021Article
- MicroRNA-137-3p Improves Nonalcoholic Fatty Liver Disease through Activating AMPKAnalytical cellular pathology (Amsterdam) · 2021Article
- Ubiquitin-Specific Protease 29 Exacerbates Cerebral Ischemia-Reperfusion Injury in Mice.Oxidative medicine and cellular longevity · 2021Article
- TLR9 deficiency alleviates doxorubicin-induced cardiotoxicity via the regulation of autophagy.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin is a commonly used anthracycline chemotherapeutic drug. Its application for treatment has been impeded by its cardiotoxicity as it is detrimental and fatal. DNA damage, cardiac inflammation, oxidative stress and cell death are the critical links in DOX-induced myocardial injury. Previous studies found that TLR9-related signalling pathways are associated with the inflammatory response of cardiac myocytes, mitochondrial dysfunction and cardiomyocyte death, but it remains unclear whether TLR9 could influence DOX-induced heart injury. Our current data imply that DOX-induced cardiotoxicity is ameliorated by TLR9 deficiency both in vivo and in vitro, manifested as improved cardiac function and reduced cardiomyocyte apoptosis and oxidative stress. Furthermore, the deletion of TLR9 rescued DOX-induced abnormal autophagy flux in vivo and in vitro. However, the inhibition of autophagy by 3-MA abolished the protective effects of TLR9 deletion on DOX-induced cardiotoxicity. Moreover, TLR9 ablation suppressed the activation of p38 MAPK during DOX administration and may promote autophagy via the TLR9-p38 MAPK signalling pathway. Our study suggests that the deletion of TLR9 exhibits a protective effect on doxorubicin-induced cardiotoxicity by enhancing p38-dependent autophagy. This finding could be used as a basis for the development of a prospective therapy against DOX-induced cardiotoxicity.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.