Targeting Chemo-Induced Cardiotoxicity via CD47 09/09/25
Welcome to Cardiology Today – Recorded September 09, 2025. This episode summarizes 3 key cardiology studies on topics like Doxorubicin-Induced Cardiomyopathy and Intracellular Receptors. Key takeaway: Targeting Chemo-Induced Cardiotoxicity via CD47.
Article Links:
Article 1: Human Single-Nucleus RNA Sequencing Identifies CD47 as a Therapeutic Target for Doxorubicin-Induced Cardiomyopathy. (Circulation)
Article 2: Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction. (Circulation)
Article 3: Unique Role of Intracellular Perinuclear β1-Adrenergic Receptors in Defining Signaling Compartmentation and Pathological Cardiac Remodeling. (Circulation)
Full episode page: https://podcast.explainheart.com/podcast/targeting-chemo-induced-cardiotoxicity-via-cd47-09-09-25/
📚 Featured Articles
Article 1: Human Single-Nucleus RNA Sequencing Identifies CD47 as a Therapeutic Target for Doxorubicin-Induced Cardiomyopathy.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40808662
Summary: This study used single-nucleus ribonucleic acid sequencing on left ventricular myocardial tissue to compare patients with doxorubicin cardiomyopathy to those with nonischemic cardiomyopathy and nonfailing hearts, finding significant transcriptional changes associated with doxorubicin cardiomyopathy. The analysis identified CD47 as a potential therapeutic target, suggesting that modulating CD47 expression could improve outcomes for patients experiencing chemotherapy-induced cardiotoxicity. These results offer a targeted approach to mitigating the adverse cardiac effects of doxorubicin.
Article 2: Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40709455
Summary: This research demonstrated that junctophilin-2, a protein known for regulating calcium signaling in cardiomyocytes, also plays a critical role in cardiac fibroblast activation after myocardial infarction. Specifically, junctophilin-2 regulates store-operated calcium entry in cardiac fibroblasts, driving fibrotic repair and angiogenesis. The study indicates that modulating junctophilin-2 expression or activity in cardiac fibroblasts could be a novel therapeutic strategy to improve myocardial healing and prevent adverse remodeling post-infarction.
Article 3: Unique Role of Intracellular Perinuclear β1-Adrenergic Receptors in Defining Signaling Compartmentation and Pathological Cardiac Remodeling.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40665895
Summary: This investigation revealed that intracellular perinuclear beta one adrenergic receptors have a distinct function in regulating cardiac signaling and pathological remodeling, separate from beta adrenergic receptors located on the plasma membrane. The study showed that these intracellular receptors contribute to adverse cardiac remodeling in disease. These findings suggest that targeting intracellular beta one adrenergic receptor signaling may offer a more specific approach to preventing or treating pathological cardiac remodeling compared to traditional beta-blocker therapies.
📝 Transcript
Today’s date is September 09, 2025. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. Human Single-Nucleus RNA Sequencing Identifies CD47 as a Therapeutic Target for Doxorubicin-Induced Cardiomyopathy. This study used single-nucleus ribonucleic acid sequencing on left ventricular myocardial tissue to compare patients with doxorubicin cardiomyopathy to those with nonischemic cardiomyopathy and nonfailing hearts, finding significant transcriptional changes associated with doxorubicin cardiomyopathy. The analysis identified CD47 as a potential therapeutic target, suggesting that modulating CD47 expression could improve outcomes for patients experiencing chemotherapy-induced cardiotoxicity. These results offer a targeted approach to mitigating the adverse cardiac effects of doxorubicin.
Article number two. Junctophilin-2 Regulates Store-Operated Calcium Entry to Drive Cardiac Fibroblast Activation, Fibrotic Repair, and Angiogenesis After Myocardial Infarction. This research demonstrated that junctophilin-2, a protein known for regulating calcium signaling in cardiomyocytes, also plays a critical role in cardiac fibroblast activation after myocardial infarction. Specifically, junctophilin-2 regulates store-operated calcium entry in cardiac fibroblasts, driving fibrotic repair and angiogenesis. The study indicates that modulating junctophilin-2 expression or activity in cardiac fibroblasts could be a novel therapeutic strategy to improve myocardial healing and prevent adverse remodeling post-infarction.
Article number three. Unique Role of Intracellular Perinuclear β1-Adrenergic Receptors in Defining Signaling Compartmentation and Pathological Cardiac Remodeling. This investigation revealed that intracellular perinuclear beta one adrenergic receptors have a distinct function in regulating cardiac signaling and pathological remodeling, separate from beta adrenergic receptors located on the plasma membrane. The study showed that these intracellular receptors contribute to adverse cardiac remodeling in disease. These findings suggest that targeting intracellular beta one adrenergic receptor signaling may offer a more specific approach to preventing or treating pathological cardiac remodeling compared to traditional beta-blocker therapies.
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🔍 Keywords
Doxorubicin-Induced Cardiomyopathy, Intracellular Receptors, G Protein-Coupled Receptors, Single-Nucleus RNA Sequencing, Cardiac Fibroblasts, Junctophilin-2, Cardiac Remodeling, Signal Compartmentation, CD47, Store-Operated Calcium Entry, Myocardial Infarction, Chemotherapy-Induced Cardiotoxicity, Fibrotic Repair, Beta One Adrenergic Receptors.
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Concise summaries of cardiovascular research for professionals.
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