ArticleBiomedicines2022
Interleukin-10 Mitigates Doxorubicin-Induced Endoplasmic Reticulum Stress as Well as Cardiomyopathy.
Article in Biomedicines, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
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Who cites it
16 citing papers in PubMed, 16 citations in OpenAlex.
- Unconventional role of hydroxymethylglutaryl-CoA synthase 1 in driving pathogenic TScience advances · 2026Article
- Article
- Research progress on coronary heart disease and cytokines: mechanisms, clinical implications, and future directions.Journal of cardiothoracic surgery · 2026Review
- Evaluation of vinpocetine in an acute doxorubicin-induced cardiotoxicity model in rats.Scientific reports · 2026Article
- Regulation of Endoplasmic Reticulum Stress by Empagliflozin in Doxorubicin-Induced Cardiotoxicity in Rats.Journal of cellular and molecular medicine · 2026Article
- ERp46 mitigates lipotoxic ER stress to preserve GLUT2 expression and insulin secretion in β-cells.Biomedical reports · 2026Article
- M2 polarization of macrophage protects the lung cancer cells from cold atmospheric plasma via alleviating endoplasmic reticulum stress.Cell death discovery · 2025Article
- Mechanisms of ferroptotic and non-ferroptotic organ toxicity of chemotherapy: protective and therapeutic effects of ginger, 6-gingerol and zingerone in preclinical studies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Cardioprotective Effects of Dapagliflozin and Trimetazidine on Doxorubicin-Induced Cardiotoxicity in Streptozotocin-Induced Type 1 Diabetic Rats via Endoplasmic Reticulum Stress.Journal of clinical medicine · 2025Article
- Endoplasmic reticulum stress in cardiomyopathies: from the unfolded protein response to therapeutic opportunities.Frontiers in cardiovascular medicine · 2025Review
- Salvianolic acid B: a promising cardioprotective agent.Frontiers in immunology · 2025Review
- α-Bisabolol: A Dietary Sesquiterpene that Attenuates Apoptotic and Nonapoptotic Cell Death Pathways by Regulating the Mitochondrial Biogenesis and Endoplasmic Reticulum Stress-Hippo Signaling Axis in Doxorubicin-Induced Acute Cardiotoxicity in Rats.ACS pharmacology & translational science · 2024Article
- Doxorubicin‑induced cardiomyopathy is mitigated by empagliflozin via the modulation of endoplasmic reticulum stress pathways.Molecular medicine reports · 2024Article
- Sex-related differences in delayed doxorubicin-induced cardiac dysfunction in C57BL/6 mice.Archives of toxicology · 2024Article
- Potential role of endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity-an update.Frontiers in pharmacology · 2024Review
- Molecular mechanisms of anthracycline induced cardiotoxicity: Zebrafish come into play.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The use of doxorubicin (Dox) in cancer patients carries the risk of cardiotoxicity via an increase in oxidative stress, mitochondrial dysfunction, and disturbed endoplasmic reticulum (ER) homeostasis in cardiomyocytes. The present study explores which of the ER transmembrane sensors is involved in Dox-induced apoptosis and whether interleukin-10 (IL-10) has any mitigating effect. There was a time-related increase in apoptosis in cardiomyocytes exposed to 5.43 µg/mL Dox for 0 to 48 h. Dox treatment for 24 h significantly upregulated glucose-regulated proteins 78 and 94, protein disulfide isomerase, cleavage of activating transcription factor 6α, and X-box binding protein 1. These Dox-induced changes in ER stress proteins as well as apoptosis were blunted by IL-10 (10 ng/mL). In Dox-exposed cardiomyocytes, IL-10 also promoted expression of protein kinase-like endoplasmic reticulum kinase and inositol-requiring kinase 1α, which helped in maintaining ER homeostasis. Additionally, under Dox-treatment, IL-10 downregulated caspase-12 activation as well as phosphorylation of c-JUN NH2-terminal kinase, thereby promoting cardiomyocyte survival. IL-10 was able to reduce the overexpression of mitochondrial apoptotic proteins caspase-3 as well as Bax, which were upregulated upon Dox treatment. Thus, a reduction in Dox-induced ER stress as well as apoptosis through IL-10 may provide a significant benefit in improving cardiac function.
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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.