🆕 in JMCC: DCBLD2 protects against calcific aortic valve disease by limiting TGF-β signaling & endothelial-to-mesenchymal transition. Enhancing DCBLD2 reduces valve calcification, highlighting a potential therapeutic target for CAVD ❤️‍🩹 www.jmcc-online.com/article/S002...

📢 Calling PhD students & postdocs! Submit your abstract for the 2026 @ISHR_NAS ECI Winter Webinar! 🗓️ Dec 10 | 11AM–3PM EST 🏆 Four $750 travel awards to ISHR-NAS 2027 ⏰ Abstract deadline: Oct 31 Register and submit your abstract today: ishrnorthamerican.org/eci/

🆕 in JMCC: Silencing PACS2 attenuates cardiac hypertrophy by increasing SIRT1, activating Nrf2/HO-1 signaling, and suppressing oxidative stress and ferroptosis, identifying PACS2 as a potential therapeutic target 🎯 www.jmcc-online.com/article/S002...

🆕 in JMCC: HDAC7 protects against pathological cardiac hypertrophy and remodeling by interacting with and repressing MEF2D. The HDAC7-MEF2D axis highlights a potential epigenetic strategy to prevent heart failure progression 💪🏼 www.jmcc-online.com/article/S002...

🆕 in JMCC: HCM mutations produce distinct metabolic phenotypes. R403Q-MyHC hearts show impaired fatty acid and pyruvate oxidation and reduced energy reserves, while R92W-TnT hearts maintain normal metabolism❤️‍🔥 www.jmcc-online.com/article/S002...

🆕 in JMCC: In coronary artery disease, anemia increases release of RBC-derived extracellular vesicles that promote endothelial dysfunction by consuming nitric oxide and delivering MPO, linking anemia to vascular oxidative stress ⚡️ www.jmcc-online.com/article/S002...

🆕 in JMCC: CRISPR-Cas9 base editing offers a new approach to heart failure by precisely modifying disease-driving signaling. Editing PKCα promotes its degradation and cardioprotection, highlighting the promise of “precision signaling modification.” ✂️ 🧬 www.jmcc-online.com/article/S002...

🆕 in JMCC: An integrated structural, biophysical, and cellular analysis supports pathogenicity of the FLNC-M82K variant linked to dilated cardiomyopathy and provides a framework for interpreting VUS in cardiomyopathy genes 🧬 www.jmcc-online.com/article/S002...

🆕 in JMCC: Returning to a normal diet improves cardiac function and reduces inflammation, fibrosis, and pyroptosis in diabetic mice. Multi-omics analyses link these benefits to suppression of JAK/STAT-dependent pyroptosis ❤️‍🔥 www.jmcc-online.com/article/S002...

🆕 in JMCC: Cardiomyocyte-targeted Gi activation protects against sustained adrenergic stress, preserving cell viability, reducing CCR2⁺ monocyte recruitment, and restoring cardiac function, highlighting a strategy to promote myocardial repair ❤️‍🩹 www.jmcc-online.com/article/S002...

🆕 in JMCC: snRNA-seq identifies the FN1-SDC4 axis as a driver of epicardial activation in pulmonary hypertension. Epicardial Sdc4 knockdown limits right ventricular remodeling, highlighting a potential therapeutic target 🎯 www.jmcc-online.com/article/S002...

🆕 in JMCC: PAI-1 deficiency drives sex-specific cardiac fibrosis after stress. Metformin reduces fibrosis and improves cardiac function in a sex- and stressor-dependent manner, with marked protection in females after AngII ♀️ www.jmcc-online.com/article/S002...

🆕 in JMCC: The deubiquitinase OTUD5 promotes pathological cardiac hypertrophy by stabilizing TRAF2 and activating NF-κB and AKT/GSK3β signaling, identifying the OTUD5-TRAF2 axis as a potential therapeutic target🎯 www.jmcc-online.com/article/S002...

🚨 New in JMCC: A KCNH2 mutation alters L-type Ca²⁺ current gating in LQT2 cardiomyocytes. Estradiol corrects key Ca²⁺ current defects and shortens repolarization, yet may paradoxically preserve susceptibility to early afterdepolarizations⚡️ www.jmcc-online.com/article/S002...

🆕 in JMCC: In vivo phosphoproteomics maps EGF- and NRG1β-driven ErbB signaling in the adult heart, revealing shared and ligand-specific networks spanning insulin signaling, Ca²⁺ handling, metabolism, and sarcomere regulation🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: SK channels become functionally active early in human ventricular remodeling despite unchanged expression. Their recruitment depends on Ca²⁺ handling and CaMKII signaling, with implications for SK-targeted AF therapies 💊 www.jmcc-online.com/article/S002...

🆕 in JMCC: Low-dose melatonin promotes coronary angiogenesis and improves cardiac function after MI by targeting endothelial LRRC8A and activating AKT/eNOS/HIF1α signaling, revealing a potential strategy for ischemic heart disease 🫀 www.jmcc-online.com/article/S002...

🚨 New in JMCC: This Letter to the Editor shows that dietary BCAA availability modifies exercise-induced cardiac growth in male mice, while improved exercise capacity can occur independently of cardiac growth in both sexes ♀️ ♂️ www.jmcc-online.com/article/S002...

🚨 New in JMCC: The C-terminal peptide of cardiac troponin T binds the thin filament and reduces Ca²⁺ sensitivity, while HCM mutations disrupt these effects, revealing a potential strategy to correct myocardial hyperactivation 💪🏼 www.jmcc-online.com/article/S002...

🆕 in JMCC: Quercetin improves cardiac redox balance and antioxidant defenses in diabetic rats but fails to restore mitochondrial respiration, suggesting antioxidant therapy alone may not reverse T2DM-related cardiac bioenergetic dysfunction ⚡️ www.jmcc-online.com/article/S002...

🚨 Please join us for our next ISHR MCI Seminar on Wednesday, September 9 featuring Drs Mingtao Zhao and John Calvert, who will share their latest research🔬🧬🫀 Register today and save your spot! us02web.zoom.us/webinar/regi...

⭐ Editor's Choice | 🆕 in JMCC: This study uncovers a stepwise mechanism of enhancer activation in plastic vascular smooth muscle cells, revealing how H2A.Z-driven enhancer maturation shapes cell plasticity and vascular remodeling throughout adult life. www.jmcc-online.com/article/S002...

🆕 in JMCC: Enhancing mitochondrial SK channels restores mitochondrial Ca²⁺ and redox homeostasis, suppresses pro-arrhythmic Ca²⁺ release, and rescues Ca²⁺ cycling in HFpEF cardiomyocytes, highlighting a promising antiarrhythmic strategy⚡️ www.jmcc-online.com/article/S002...

🚨 New in JMCC: This review highlights how single-cell multi-omics and computational approaches are transforming our understanding of cardiac aging, revealing cell type-specific remodeling and new therapeutic targets in aging hearts 💊 ❤️‍🩹 www.jmcc-online.com/article/S002...

🆕 in JMCC: L-menthol protects cardiomyocytes from lipid overload by preserving TRPM8 signaling, mitochondrial Ca²⁺ homeostasis, and mitochondrial function. Stabilizing TRPM8 may represent a new therapeutic strategy for metabolic heart disease🫀 www.jmcc-online.com/article/S002...

🚨 New in JMCC: Integrated single-cell multi-omics identifies fibroblast-like smooth muscle cells as a progenitor-like population driving aortic aneurysm progression through a KAT5-mediated metabolism-epigenetic axis regulating phenotypic switching 🧬 www.jmcc-online.com/article/S002...

🆕 in JMCC: A CRISPR-generated non-phosphorylatable phospholamban (PLB) mouse model reveals that PLB phosphorylation is essential for a full adrenergic response, preserving SR Ca²⁺ load, Ca²⁺ reuptake, and excitation-contraction coupling ⚡️ www.jmcc-online.com/article/S002...

New in JMCC! Zu and colleagues uncover the functional divergence of hoxb5 paralogues, identifying hoxb5a as the dominant regulator of cardiac morphogenesis and calcium handling in vertebrate heart development. www.jmcc-online.com/article/S002...

Evolutionary differentiation of duplicated hoxb5 paralogs orchestrates calcium signaling and contractility

hox genes are evolutionarily conserved transcription factors essential for anterior–posterior body patterning, yet their specific contributions to cardiac morphogenesis and calcium signaling remain…

jmcc-online.com

New in JMCC! Phosphorylation of βIII-tubulin at Ser172 restores microtubule network organization and protects against arrhythmias and cardiac fibrosis in Duchenne muscular dystrophy cardiomyopathy. www.jmcc-online.com/article/S002...

Phospho-mimic βIII-tubulin rescues microtubule and cardiac defects in Duchenne muscular dystrophy mice

Duchenne muscular dystrophy (DMD) cardiomyopathy is caused by mutations in the dystrophin gene and characterized by profound cytoskeletal disorganization, particularly pathological remodeling of the…

jmcc-online.com

New in JMCC! A five small molecule cocktail (5SM) promotes cardiac regeneration post-MI via activation of the DYRK1B–PKA–CREB–TGFβ/BMP signaling axis. www.jmcc-online.com/article/S002...

Small-molecule cocktail 5SM induces heart regeneration by upregulating TGFβ/BMP signaling

Zebrafish and neonatal mammals possess a remarkable capacity for cardiac regeneration following injury, a property that is largely absent in adult mammals. We have recently identified a cocktail of…

jmcc-online.com