ArticleMedical science monitor : international medical journal of experimental and clinical research2019
MD-1 Deficiency Accelerates Myocardial Inflammation and Apoptosis in Doxorubicin-Induced Cardiotoxicity by Activating the TLR4/MAPKs/Nuclear Factor kappa B (NF-κB) Signaling Pathway.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 19 citations in OpenAlex.
- Retracted: MD-1 Deficiency Accelerates Myocardial Inflammation and Apoptosis in Doxorubicin-Induced Cardiotoxicity by Activating the TLR4/MAPKs/Nuclear Factor kappa B (NF-κB) Signaling Pathway.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy.Cell communication and signaling : CCS · 2023Review
- Upregulation of Biomarker Limd1 Was Correlated with Immune Infiltration in Doxorubicin-Related Cardiotoxicity.Mediators of inflammation · 2023Article
- Oxidative Stress and Pyroptosis in Doxorubicin-Induced Heart Failure and Atrial Fibrillation.Oxidative medicine and cellular longevity · 2023Article
- SIRT1 activation and its effect on intercalated disc proteins as a way to reduce doxorubicin cardiotoxicity.Frontiers in pharmacology · 2022Review
- Inflammation suppression in doxorubicin-induced cardiotoxicity: natural compounds as therapeutic options.Naunyn-Schmiedeberg's archives of pharmacology · 2021Review
- Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways.Cellular and molecular life sciences : CMLS · 2021Review
- Piperine protects against pyroptosis in myocardial ischaemia/reperfusion injury by regulating the miR-383/RP105/AKT signalling pathway.Journal of cellular and molecular medicine · 2021Article
- Anthracycline-Related Heart Failure: Certain Knowledge and Open Questions : Where Do we Stand with Chemotherapyinduced Cardiotoxicity?Current heart failure reports · 2020Review
Corrections and comments
- Retraction · 2024-05-22Concerns/Issues about Data · Concerns/Issues about Image · Concerns/Issues about Results and/or Conclusions ·
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Myocardial apoptosis and inflammation play important roles in doxorubicin (DOX)-caused cardiotoxicity. Our prior studies have characterized the effects of myeloid differentiation protein 1(MD-1) in pathological cardiac remodeling and myocardial ischemia/reperfusion (I/R) injury, but its participations and potential molecular mechanisms in DOX-caused cardiotoxicity remain unknown. MATERIAL AND METHODS In the present study, MD-1 knockout mice were generated, and a single intraperitoneal injection of DOX (15 mg/kg) was performed to elicit DOX-induced cardiotoxicity. Cardiac function, histological change, mitochondrial structure, myocardial death, apoptosis, inflammation, and molecular alterations were measured systemically. RESULTS The results showed that the protein and mRNA levels of MD-1 were dramatically downregulated in DOX-treated cardiomyocytes. DOX insult markedly accelerated cardiac dysfunction and injury, followed by enhancements of apoptosis and inflammation, all of which were further aggravated in MD-1 knockout mice. Mechanistically, the TLR4/MAPKs/NF-kappaB pathways, which were over-activated in MD-1-deficient mice, were significantly increased in DOX-damaged cardiomyocytes. Moreover, the abolishment of TLR4 or NF-kappaB via a specific inhibitor exerted protective effects against the adverse effects of MD-1 loss on DOX-caused cardiotoxicity. CONCLUSIONS Collectively, these findings suggest that MD-1 is a novel target for the treatment of DOX-induced cardiotoxicity.
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Registered trials
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.