ArticleCellular and molecular life sciences : CMLS2023
Infiltrating macrophages amplify doxorubicin-induced cardiac damage: role of catecholamines.
Article in Cellular and molecular life sciences : CMLS, 2023. 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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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Cardiomyocyte-macrophage cross-talk reduces doxorubicin cardiotoxicity by polarizing macrophages via EV miR-142-3p/135a-5p.iScience · 2026Article
- The possible effects of folic acid and postbiotic yeast on doxorubicin-induced cardiotoxicity in rats: interactions among the gut microbiota, antioxidants, and NLrp3 activities.Journal of molecular histology · 2026Article
- The mechanisms and therapeutic advances of interactions between breast cancer and cardiovascular diseases.Frontiers in pharmacology · 2026Review
- PHB1 Attenuates Triptolide-induced Cardiotoxicity by Regulating Mitochondrial Dynamics in Cultured Newborn Mice Cardiomyocytes.Journal of cardiovascular pharmacology · 2026Article
- Nano-therapeutics targeting the macrophage-based microenvironment in the treatment of atherosclerosis.Journal of translational medicine · 2025Review
- Macrophages in Cardiotoxicity: Key Mediators of Cardiac Dysfunction.JACC. Basic to translational science · 2025Article
- SLAMF7 Restrains Pro-Inflammatory Macrophage Activation to Counteract Doxorubicin-Induced Cardiotoxicity.JACC. Basic to translational science · 2025Article
- Doxorubicin-Induced Cardiotoxicity: A Comprehensive Update.Journal of cardiovascular development and disease · 2025Review
- Article
- Sodium-glucose cotransporter 2 inhibitors and the cancer patient: from diabetes to cardioprotection and beyond.Basic research in cardiology · 2025Review
- Cardiomyocyte GSDME Drives Doxorubicin-Induced Cardiotoxicity by Targeting the CCL2-CCR2 Axis.International journal of biological sciences · 2025Article
- Clinicopathological Studies on the Impact of Grape Seed Extract and L-Carnitine as Cardioprotective Agents Against Doxorubicin-Induced Toxicity in Rats.Life (Basel, Switzerland) · 2024Article
- Oxidative Stress and Inflammation in Cancer.Antioxidants (Basel, Switzerland) · 2024Article
- Review
- Natural Products for Preventing and Managing Anthracycline-Induced Cardiotoxicity: A Comprehensive Review.Cells · 2024Review
- Changes in blood metabolomes as potential markers for severity and prognosis in doxorubicin-induced cardiotoxicity: a study in HER2-positive and HER2-negative breast cancer patients.Journal of translational medicine · 2024Article
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundThe functional contribution of non-myocyte cardiac cells, such as inflammatory cells, in the setup of heart failure in response to doxorubicin (Dox) is recently becoming of growing interest.
objectivesThe study aims to evaluate the role of macrophages in cardiac damage elicited by Dox treatment.
methodsC57BL/6 mice were treated with one intraperitoneal injection of Dox (20 mg/kg) and followed up for 5 days by cardiac ultrasounds (CUS), histological, and flow cytometry evaluations. We also tested the impact of Dox in macrophage-depleted mice. Rat cardiomyoblasts were directly treated with Dox (D-Dox) or with a conditioned medium from cultured murine macrophages treated with Dox (M-Dox).
resultsIn response to Dox, macrophage infiltration preceded cardiac damage. Macrophage depletion prevents Dox-induced damage, suggesting a key role of these cells in promoting cardiotoxicity. To evaluate the crosstalk between macrophages and cardiac cells in response to DOX, we compared the effects of D-Dox and M-Dox in vitro. Cell vitality was lower in cardiomyoblasts and apoptosis was higher in response to M-Dox compared with D-Dox. These events were linked to p53-induced mitochondria morphology, function, and autophagy alterations. We identify a mechanistic role of catecholamines released by Dox-activated macrophages that lead to mitochondrial apoptosis of cardiac cells through β-AR stimulation.
conclusionsOur data indicate that crosstalk between macrophages and cardiac cells participates in cardiac damage in response to Dox.
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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 Socratic graph.