Collagen-Derived Dipeptide Pro-Hyp Administration Accelerates Muscle Regenerative Healing Accompanied by Less Scarring after Wounding on the Abdominal Wall in Mice

Pro-Hyp administration induced many myogenically differentiated cells, including myogenin-positive myoblasts and myoglobin-positive myocytes, to migrate in the granulation tissue, while scar tissue decreased, indicating that Pro-Hyp administration accelerated muscle regenerative healing accompanied by less scarring after wounding on the abdominal wall.
[Scientific Reports]
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Hemicentin-1 Is an Essential Extracellular Matrix Component of the Dermal–Epidermal and Myotendinous Junctions

Performing in situ hybridization and immunofluorescence analysis, researchers found that mouse Hmcn1 and Hmcn2 showed a complementary distribution throughout different tissues and developmental stages.
[Scientific Reports]
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The Hippo Pathway Regulates Density-Dependent Proliferation of iPSC-Derived Cardiac Myocytes

The Hippo pathway regulates the proliferation of cancer cells, pluripotent stem cells, and epithelial cells through a cell–cell contact-dependent manner, however, it is unclear if cell density-dependent cell proliferation is a consistent feature in cardiac myocytes. Scientists used cultured human iPSC-derived cardiac myocytes as a model system to investigate this concept.
[Scientific Reports]
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Hepatocyte-Derived Exosomes from Early Onset Obese Mice Promote Insulin Sensitivity through miR-3075

FA2H was a direct target of miR-3075 and small interfering RNA depletion of FA2H in adipocytes, myocytes and primary hepatocytes led to increased insulin sensitivity. In chronic obesity, hepatocyte exosomes promoted a state of insulin resistance.
[Nature Metabolism]
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Tissue-Engineered Esophagus: Recellular Esophageal Extracellular Matrix Based on Perfusion-Decellularized Technique and Mesenchymal Stem Cells

In this study, the esophageal extracellular matrix scaffold was successfully constructed by perfusion-decellularized technique through the vascular system for the first time.
[Biomedical Materials]
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Towards Engineering Heart Tissues from Bioprinted Cardiac Spheroids

Cardiac spheroids were created from human cardiac myocytes, fibroblasts and endothelial cells, mixed within optimal alginate/gelatin hydrogels and then bioprinted on a microelectrode plate for drug testing.
[Biofabrication]
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Carbonic Anhydrase III Attenuates Hypoxia-Induced Apoptosis and Activates PI3K/Akt/mTOR Pathway in H9c2 Cardiomyocyte Cell Line

To investigate the role of CAIII in the apoptosis of myocytes under hypoxic conditions and facilitate the strategy for treating hypoxia-induced damage, in vitro experiments in H9c2 were employed.
[Cardiovascular Toxicology]
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Responsiveness to Perturbations Is a Hallmark of Transcription Factors That Maintain Cell Identity In Vitro

Investigators developed perturbation panel profiling as a framework for perturbing cells across many conditions and measuring gene expression responsiveness transcriptome-wide.
[Cell Systems]
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Cardiac-Specific Deletion of Voltage Dependent Anion Channel 2 Leads to Dilated Cardiomyopathy by Altering Calcium Homeostasis

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.
[Nature Communications]
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Transcriptome Analysis Using Patient iPSC-Derived Skeletal Myocytes: Bet1L as a New Molecule Possibly Linked to Neuromuscular Degeneration in ALS

To study common disease mechanisms in amyotrophic lateral sclerosis (ALS) skeletal muscle, the authors performed RNA sequencing of skeletal myocytes differentiated from induced pluripotent stem cells derived from familial ALS and sporadic ALS patients.
[Experimental Neurology]
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IRE1α Regulates Skeletal Muscle Regeneration through Myostatin mRNA Decay

Researchers found in mice that IRE1α was activated during injury-induced muscle regeneration, and muscle-specific IRE1α ablation resulted in impaired regeneration upon cardiotoxin-induced injury.
[Journal of Clinical Investigation]
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