Activation of Autophagic Flux Blunts Cardiac Ischemia/Reperfusion Injury

Cultured neonatal rat ventricular myocytes (NRVMs) were exposed to Tat-Beclin during simulated ischemia/reperfusion injury. ATG7 knockdown by siRNA in NRVMs was used to evaluate the role of autophagy.
[Circulation Research]
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Heartseed Raises $37 Million in Series C Funding to Accelerate Development of iPSC-Derived Stem Cell Therapy for Heart Failure

Heartseed, Inc., a biotechnology company developing iPSC-derived cardiomyocytes for heart failure, announced it has raised approx. $37 Million at Series C round. These funds will accelerate the initiation of a global clinical trial of HS-001, an allogeneic iPSC-derived, highly purified ventricular cardiomyocyte spheroids for heart failure.
[Heartseed, Inc.]
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Nanomechanical Phenotypes in Cardiac Myosin-Binding Protein C Mutants That Cause Hypertrophic Cardiomyopathy

Researchers examined whether pathogenic mutations perturbed the nanomechanics of cardiac myosin-binding protein C, which would compromise its modulatory mechanical tethers across sliding actomyosin filaments.
[ACS Nano]
AbstractGraphical Abstract
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Heartseed and Novo Nordisk Enter into Global Collaboration and Licence Agreement for Stem Cell-Based Therapy for Heart Failure

Heartseed Inc. and Novo Nordisk A/S announced that they have entered into a collaboration and licence agreement for the development, manufacturing and commercialisation of Heartseed’s asset HS-001, an investigational cell therapy using purified cardiomyocytes derived from induced pluripotent stem cells, which is currently under development by Heartseed for the treatment of heart failure.
[Heartseed, Inc.]
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Engineering Aligned Human Cardiac Muscle Using Developmentally Inspired Fibronectin Micropatterns

Scientists identified cell–cell and cell-ECM interactions in the microenvironment of the early four-chambered vertebrate heart that drive cardiomyocyte organization and alignment.
[Scientific Reports]
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Remodeling of T-System and Proteins Underlying Excitation-Contraction Coupling in Aging versus Failing Human Heart

Researchers showed that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age, characterized by t-system alterations and sarcolemmal dissociation of ryanodine receptor clusters.
[npj Aging and Mechanisms of Disease]
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A Human Antibody Selective for Transthyretin Amyloid Removes Cardiac Amyloid through Phagocytic Immune Cells

Scientists developed the selective anti-Transthyretin amyloid antibody NI301A, a recombinant human monoclonal immunoglobulin G1.
[Nature Communications]
Michalon, A., Hagenbuch, A., Huy, C., Varela, E., Combaluzier, B., Damy, T., Suhr, O. B., Saraiva, M. J., Hock, C., Nitsch, R. M., & Jan Grimm. (2021). A human antibody selective for transthyretin amyloid removes cardiac amyloid through phagocytic immune cells. Nature Communications, 12(1), 3142. https://doi.org/10.1038/s41467-021-23274-x Cite
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Adropin-Based Dual Treatment Enhances the Therapeutic Potential of Mesenchymal Stem Cells in Rat Myocardial Infarction

Adropin in vitro reduced hydrogen peroxide-induced apoptosis in rat bone marrow MSCs and improved MSCs survival with increased phosphorylation of Akt and extracellular regulated protein kinases.
[Cell Death & Disease]
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Circular RNA circACSL1 Aggravated Myocardial Inflammation and Myocardial Injury by Sponging miR-8055 and Regulating MAPK14 Expression

Researchers determined a novel circRNA, circACSL1, which was significantly upregulated in the acute phase of myocarditis, by using lipopolysaccharide to induce inflammatory responses in the human cardiomyocytes line.
[Cell Death & Disease]
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Neuregulin-1 Compensates for Endothelial Nitric Oxide Synthase Deficiency

Scientists hypothesized that NRG1 could compensate for endothelial nitric oxide (NO) synthase (eNOS) deficiency. Methods. They characterized eNOS null and wild type mice by cardiac ultrasound and histology and determined circulating NRG1 levels.
[American Journal of Physiology-Heart and Circulatory Physiology]
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Phenotypic Recapitulation and Correction of Desmoglein-2-Deficient Cardiomyopathy using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes

Scientists identified a homozygous stop-gain mutations in DSG2 that led to complete desmoglein-2 deficiency in a patient with severe biventricular heart failure. Induced pluripotent stem cells were generated from the patient, and the mutated DSG2 gene locus was heterozygously corrected to a normal allele via homology-directed repair.
[Human Molecular Genetics]
Shiba, M., Higo, S., Kondo, T., Li, J., Liu, L., Ikeda, Y., Kohama, Y., Kameda, S., Tabata, T., Inoue, H., Nakamura, S., Takeda, M., Ito, E., Takashima, S., Miyagawa, S., Sawa, Y., Hikoso, S., & Sakata, Y. (2021). Phenotypic Recapitulation and Correction of Desmoglein-2-deficient Cardiomyopathy using Human Induced Pluripotent Stem Cell-derived Cardiomyocytes. Human Molecular Genetics, ddab127. https://doi.org/10.1093/hmg/ddab127 Cite
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