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cardiomyocytes

Thbs1 Induces Lethal Cardiac Atrophy through PERK-ATF4 Regulated Autophagy

[Nature Communications] Researchers identified thrombospondin (Thbs)1-mediated PERK-eIF2α-ATF4-induced autophagy as a critical regulator of cardiomyocyte size in the stressed heart.

Hypertrophic Preconditioning Attenuates Post-Myocardial Infarction Injury through Deacetylation of Isocitrate Dehydrogenase 2

[Acta Pharmacologica Sinica] Expression of an IDH2 mutant mimicking deacetylation in cardiomyocytes promoted myocardial IDH2 activation, quenched mitochondrial reactive oxygen species (ROS), and alleviated post-myocardial infarction (MI) injury, whereas expression of an acetylation mimic in cardiomyocytes inactivated IDH2, exacerbated mitochondrial ROS overload, and aggravated post-MI injury.

Ischemic Heart Injury Leads to HIF1-Dependent Differential Splicing of CaMK2γ

[Scientific Reports] Investigators developed a mouse model in which a mutated form of HIF1α could be inducibly expressed in cardiomyocytes, and suggested that loss of calcium/calmodulin dependent protein kinase II, gamma (CAMK2G) after myocardial infarction was HIF1-dependent and may have played an important role in the heart’s calcium signaling and response to hypoxia.

ERRγ Enhances Cardiac Maturation with T-Tubule Formation in Human iPSC-Derived Cardiomyocytes

[Nature Communications] Scientists generated human induced pluripotent stem cells (hiPSCs) carrying a TNNI1EmGFP and TNNI3mCherry double reporter to monitor and isolate mature sub-populations during cardiac differentiation, and showed that ERRγ-treated hiPSC-cardiomyocytes (CMs) had a mature cellular property consistent with neonatal CMs.

Emodin Alleviates LPS-Induced Myocardial Injury through Inhibition of NLRP3 Inflammasome Activation

[Phytotherapy Research] Researchers investigated the protective effect of emodin on septic myocardial injury and the underlying mechanism. Lipopolysaccharide (LPS)-induced C57BL/6 mice and cardiomyocytes were used as models of sepsis in vivo and in vitro, respectively.

Control of Cardiomyocyte Differentiation Timing by Intercellular Signaling Pathways

[Seminars in Cell & Developmental Biology] The authors discuss the action of signaling pathways in the control of cardiomyocyte differentiation timing, including the Wnt, Fibroblast Growth Factor, Hedgehog, Bone Morphogenetic Protein, Insulin-like Growth Factor, Thyroid Hormone and Hippo pathways.

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