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myocardium

Exosomal Micro‐RNA‐96 Derived From Bone Marrow Mesenchymal Stem Cells Inhibits Doxorubicin‐Induced Myocardial Toxicity by Inhibiting the Rac1/Nuclear Factor‐κB Signaling Pathway

[Journal of the American Heart Association] Researchers investigated the functional mechanism of exosomal microRNA‐96 derived from bone marrow mesenchymal stem cells in myocardial toxicity induced by doxorubicin.

Protocatechuic Acid Attenuates Isoproterenol-Induced Cardiac Hypertrophy via Downregulation of ROCK1–Sp1–PKCγ Axis

[Scientific Reports] The authors demonstrated that protocatechuic acid treatment significantly downregulated the expression of cardiac hypertrophic markers, cardiomyocyte size, heart weight to body weight ratio, cross-sectional area, and thickness of left ventricular septum and posterior wall.

Electrophysiological Engineering of Heart-Derived Cells with Calcium-Dependent Potassium Channels Improves Cell Therapy Efficacy for Cardioprotection

[Nature Communications] Scientists tested the participation of calcium-activated potassium-channels in human heart explant-derived cell physiology and therapeutic potential.

A microRNA Program Regulates the Balance between Cardiomyocyte Hyperplasia and Hypertrophy and Stimulates Cardiac Regeneration

[Nature Communications] Researchers reported that the miR-106b~25 cluster was higher expressed in the early postnatal myocardium and decreased in expression towards adulthood, especially under conditions of overload, and orchestrated the transition of cardiomyocyte hyperplasia towards cell cycle arrest and hypertrophy by virtue of its targetome.

Hepatic Cell Mobilization for Protection against Ischemic Myocardial Injury

[Scientific Reports] Scientists reported a distant cardioprotective mechanism involving hepatic cell mobilization to the ischemic myocardium in response to experimental myocardial ischemia–reperfusion injury.

Cardiac-Specific Deletion of Voltage Dependent Anion Channel 2 Leads to Dilated Cardiomyopathy by Altering Calcium Homeostasis

[Nature Communications] Scientists generated a cardiac ventricular myocyte-specific developmental deletion of Vdac2 in mice and indicated that loss of VDAC2 in the myocardium caused severe impairment in excitation-contraction coupling by altering both intracellular and mitochondrial calcium signaling.

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