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…

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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…

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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…

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New in JMCC! Transient expression of OCT4, SOX2, and KLF4 enhances post-MI cardiac regeneration by promoting cardiomyocyte dedifferentiation. www.jmcc-online.com/article/S002...

OSK-mediated partial reprogramming induces cardiomyocyte dedifferentiation, overcomes cytokinesis barriers, and promotes post-MI endogenous cardiac regeneration

Myocardial infarction (MI) leads to irreversible loss of cardiomyocytes (CMs), owing to the limited regenerative capacity of the adult mammalian heart. Previous studies indicate that the Yamanaka…

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New in JMCC! This review provides an overview of the mechanisms linking metabolic syndrome to cardiovascular disease and emerging therapeutic strategies to reduce cardiovascular risk. www.jmcc-online.com/article/S002...

Pathophysiology and pharmacotherapy of cardiovascular complications in metabolic syndrome

Metabolic syndrome (MetS) symbolises a cluster of interrelated risk factors including central obesity, dyslipidemia, insulin resistance and hypertension, those significantly increase the risk of…

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New in JMCC! Lycorine hydrochloride attenuates neointimal hyperplasia and suppresses PDGF-BB-induced vascular smooth muscle cell phenotypic switching via a MAPK-dependent mechanism. www.jmcc-online.com/article/S002...

Lycorine hydrochloride reveals a novel role in preventing neointimal hyperplasia through MAPK-mediated phenotypic switching of smooth muscle cells

Neointimal hyperplasia results from irregular vascular smooth muscle cell (VSMC) proliferation and migration. Lycorine hydrochloride (LH), known for its cardioprotective properties, was investigated…

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New in JMCC! Contrary to preclinical models, JPH2 protein abundance is not reduced in failing human hearts despite significant T-tubule remodeling, highlighting the need for human tissue-based validation of candidate therapeutic targets. www.jmcc-online.com/article/S002...

Junctophilin-2 abundance is unaltered in human heart failure samples with disrupted T-tubules and contractility

T-tubules are structural components of the cardiomyocyte plasma membrane that are imperative for efficient excitation-contraction coupling and cardiac contraction. Junctophilin-2 (JPH2) has been…

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🆕in JMCC: Peroxisomes are critical regulators of lipid metabolism, redox balance, & cellular homeostasis, yet their roles in the 🫀 remain underexplored. This review by Rungreang et al highlights emerging evidence linking peroxisomes to cardiac health and disease www.jmcc-online.com/article/S002...

🆕 in JMCC: Roman et al. uncover a mechanism underlying sex differences in cardiac ischemia/reperfusion injury. Increased S-nitrosylation of MCU in female hearts limits mitochondrial calcium accumulation during ischemia♀️♂️🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: Zhou et al. reveal strikingly similar metabolic signatures in human end-stage ischemic and nonischemic cardiomyopathy. Both exhibit altered amino acid metabolism, oxidative stress, purine breakdown, and depleted glutathione ⚡️🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: Liu et al. identify hematopoietic PI3Kγ as a key driver of abdominal aortic aneurysm progression. PI3Kγ promotes macrophage trafficking, aortic inflammation, and aneurysm growth, highlighting a potential therapeutic target 🎯 www.jmcc-online.com/article/S002...

🚨 New in JMCC: Jiang et al. identify the CYLD-RIPK1 axis as a key regulator of DNA damage and pathological cardiac hypertrophy. Targeting CYLD attenuated remodeling and preserved cardiac function in pressure-overloaded hearts 🎯 www.jmcc-online.com/article/S002...

🆕 in JMCC: Bacchini et al. show that aging and cardiomyopathy jointly reshape unfolded protein response pathways, highlighting defective proteostasis as a key contributor to myocardial dysfunction and heart failure 👴🏼👵🏼🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: PERK is a key regulator of the unfolded protein response, but its activation mechanisms remain unclear. Georgoula et al. identify stable PERK assembly states that persist during ER stress, suggesting new modes of regulation 👏🏼 www.jmcc-online.com/article/S002...

🆕 in JMCC Special Issue on The Diabetic Heart: Kanki and Young review the role of mineralocorticoid receptor signaling in diabetic cardiomyopathy and its potential as a therapeutic target to reduce cardiovascular risk 🫀 💪🏼 www.jmcc-online.com/article/S002...

🚨 New in JMCC: Zheng et al. identify DPP4 as a key regulator of endothelial ferroptosis in atherosclerosis. DPP4 promotes ferritinophagy, endothelial dysfunction, and plaque progression, highlighting a potential therapeutic target 🎯 www.jmcc-online.com/article/S002...

🚨 New in JMCC: Zhang et al. identify LARP7 as a regulator of cardiomyocyte proliferation and cardiac regeneration. LARP7 promotes G2/M transition and, with CDK4/CCND1, improves heart repair after injury ❤️‍🩹 www.jmcc-online.com/article/S002...

🚨 New in JMCC! Ventricular arrythmias drive sudden cardiac death after MI. Zhou et al. show that reducing KCNQ2 in stellate ganglion neurons worsens these arrythmias. www.jmcc-online.com/article/S002...

KCNQ2 downregulation in left stellate ganglion neurons exacerbates malignant ventricular arrhythmias after myocardial infarction

Ventricular arrhythmias (VAs) are a leading cause of sudden cardiac death (SCD) following myocardial infarction (MI), with cardiac sympathetic hyperexcitability serving as a critical trigger. While…

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🚨 New in JMCC! The GWAS-identified CAD risk gene and transcription factor PRDM16 is a key regulator of VSMC homeostasis, promoting proliferation and neointima formation by repressing Tgfb2 expression. www.jmcc-online.com/article/S002...

Coronary artery disease risk gene PRDM16 regulates smooth muscle homeostasis

Vascular smooth muscle cells (VSMCs) are the primary contractile component of blood vessels and can undergo phenotypic switching from a contractile to a synthetic phenotype in vascular diseases such…

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🚨 New in JMCC! Paired human LV and RV biopsy metabolomics reveal that ischemia-reperfusion causes greater metabolic depletion in the LV, especially during CABG, highlighting ventricle-specific vulnerabilities in cardiac surgery. www.jmcc-online.com/article/S002...

Left and right myocardial ventricular energetics during cardioplegic ischemic arrest and reperfusion in patients undergoing cardiac surgery

Effective myocardial protection during cardiac surgery is essential, yet the differential metabolic stress of the left (LV) and right ventricles (RV) to ischemia–reperfusion remains poorly…

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🚨 New in JMCC! Multi-omics approaches reveal that impaired VSMC TGF-β signaling drives mitochondrial dysfunction, contributing to the pathogenesis of thoracic aortic aneurysm and dissection. www.jmcc-online.com/article/S002...

Tgfbr2 deficiency promotes mitochondrial dysfunction of vascular smooth muscle cells in thoracic aortic aneurysms and dissections

Mitochondrial dysregulation promotes vascular destabilization through modulation of the phenotypic plasticity of vascular smooth muscle cells (VSMCs) in thoracic aortic aneurysms and dissections…

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🚨 New in JMCC! CDNF’s C-domain drives potent cardioprotection via PI3K/Akt signaling and mediates ER stress–dependent KDEL receptor binding, while the N-domain is essential for CDNF internalization. www.jmcc-online.com/article/S002...

The C-domain of the cerebral dopamine neurotrophic factor (CDNF) is responsible for its cardioprotective activity by binding to the KDEL receptor relocated to the plasma membrane under endoplasmic reticulum stress conditions

Cerebral dopamine neurotrophic factor (CDNF) has emerged as a key cytoprotective molecule, with well-documented neuroprotective effects in Parkinson's disease models and, more recently, demonstrated…

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🆕in JMCC: Single-cell analyses reveal activated, dysfunctional cardiac T cells in dilated cardiomyopathy. Distinct CD4⁺ subsets, including tissue-resident memory T cells, show pro-fibrotic signaling linked to ERα activity and systolic dysfunction 🫀 www.jmcc-online.com/article/S002...

🆕in JMCC: AAV-mediated delivery of WT TNNI3 rescues thin filament-mediated dilated cardiomyopathy in a murine model of Tnni3 mutation. Gene supplementation restored troponin function and prevented the development of heart failure🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: Transcription initiation factor TIF-1A regulates vascular smooth muscle contraction and blood pressure by controlling ribosome biogenesis. Smooth muscle-specific Tif-1a loss reduces vasoconstriction and protects against Ang II-induced hypertension 💪🏼 www.jmcc-online.com/article/S002...

🆕 in JMCC: Atrial t-tubules undergo dynamic postnatal remodeling as Ca²⁺ handling matures. Despite structural changes and reduced ICa-L and SR Ca²⁺, decreased Ca²⁺ buffering helps preserve Ca²⁺ transients during development 🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: JTC801 suppresses HIF-1α–mediated CA9 activation to trigger alkaliptosis in vascular smooth muscle cells, restoring intracellular pH homeostasis and reducing aortic dissection formation in a mouse model 👏🏼 www.jmcc-online.com/article/S002...

Check out this 🆕 article in JMCC: METTL3-driven m6A modification enhances LGMN translation via YTHDF1, promoting macrophage ferroptosis and accelerating atherosclerosis. Targeting this pathway may offer new therapeutic opportunities 🫀 www.jmcc-online.com/article/S002...

🆕 in JMCC: Genetically encoded biosensors reveal real-time redox dynamics in cytosol and mitochondria of live cells. The study shows metabolic pathways shape compartmental redox balance and that mitochondrial redox status is highly sensitive to stress ⚡️ www.jmcc-online.com/article/S002...

🆕 in JMCC: Acetylation of ACTC1 at K326 and K328 weakens actin-tropomyosin interactions and reduces thin filament inhibition under low Ca²⁺, promoting contractile activation. New work reveals how actin modification can tune cardiac thin filament regulation 🫀 🦾 www.jmcc-online.com/article/S002...