Optogenetic Current in Myofibroblasts Acutely Alters Electrophysiology and Conduction of Co-Cultured Cardiomyocytes

Cardiac myofibroblasts were transduced with Channelrhodopsin-2, which allowed acute and selective increase of myofibroblast current, and plated on top of cardiomyocytes.
[Scientific Reports]
Kostecki, G. M., Shi, Y., Chen, C. S., Reich, D. H., Entcheva, E., & Tung, L. (2021). Optogenetic current in myofibroblasts acutely alters electrophysiology and conduction of co-cultured cardiomyocytes. Scientific Reports, 11(1), 4430. https://doi.org/10.1038/s41598-021-83398-4 Cite
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Exercise Triggers CAPN1-Mediated AIF Truncation, Inducing Myocyte Cell Death in Arrhythmogenic Cardiomyopathy

When cardiomyocytes differentiated from Dsg2mut/mut embryonic stem cells were challenged with β-adrenergic stimulation, calpain-1 (CAPN1) inhibition attenuated CAPN1-induced AIF truncation.
[Science Translational Medicine]
Chelko, S. P., Keceli, G., Carpi, A., Doti, N., Agrimi, J., Asimaki, A., Beti, C. B., Miyamoto, M., Amat-Codina, N., Bedja, D., Wei, A.-C., Murray, B., Tichnell, C., Kwon, C., Calkins, H., James, C. A., O’Rourke, B., Halushka, M. K., Melloni, E., … Paolocci, N. (2021). Exercise triggers CAPN1-mediated AIF truncation, inducing myocyte cell death in arrhythmogenic cardiomyopathy. Science Translational Medicine, 13(581). https://doi.org/10.1126/scitranslmed.abf0891 Cite
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Bioengineering the Extracellular Matrix to Improve the Cellular and Molecular Physiology of Cells In Vitro

The authors present a novel biomimetic substrate with submicron topographies that is capable of mimicking the mechanical and structural cues of the ECM while benefiting from high-precision, easy-to-reproduce, and scalable photolithography-based fabrication techniques.
[Biophysical Journal]
Ghazizadeh, H., Fisher, E. C., Gray, K., Smith, A. S., Kim, D.-H., & Geisse, N. (2021). Bioengineering the Extracellular Matrix to Improve the Cellular and Molecular Physiology of Cells In Vitro. Biophysical Journal, 120(3), 88a. https://doi.org/10.1016/j.bpj.2020.11.739 Cite
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MEF2C Shapes the Microtranscriptome during Differentiation of Skeletal Muscles

Deep sequencing of small RNAs of human muscle cells revealed a set of miRNAs, including several muscle-specific miRNAs, that were sensitive to myocyte enhancer factor 2C (MEF2C) depletion.
[Scientific Reports]
Piasecka, A., Sekrecki, M., Szcześniak, M. W., & Sobczak, K. (2021). MEF2C shapes the microtranscriptome during differentiation of skeletal muscles. Scientific Reports, 11(1), 3476. https://doi.org/10.1038/s41598-021-82706-2 Cite
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Elevated Myocardial Fructose and Sorbitol Levels Are Associated with Diastolic Dysfunction in Diabetic Patients, and Cardiomyocyte Lipid Inclusions In Vitro

Scientists clinically evaluated links between myocardial fructose and sorbitol levels with evidence of cardiac dysfunction, and to experimentally assess the cardiomyocyte mechanisms involved in mediating the metabolic effects of elevated fructose.
[Nutrition & Diabetes]
Daniels, L. J., Annandale, M., Koutsifeli, P., Li, X., Bussey, C. T., van Hout, I., Bunton, R. W., Davis, P. J., Coffey, S., Katare, R., Lamberts, R. R., Delbridge, L. M. D., & Mellor, K. M. (2021). Elevated myocardial fructose and sorbitol levels are associated with diastolic dysfunction in diabetic patients, and cardiomyocyte lipid inclusions in vitro. Nutrition & Diabetes, 11(1), 1–7. https://doi.org/10.1038/s41387-021-00150-7 Cite
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Microfibrillar-Associated Protein 4 Regulates Stress-Induced Cardiac Remodeling

Scientists identified a novel role for a non-myocyte-derived and TGFbeta1-induced extracellular matrix protein microfibrillar-associated protein 4 in the pathophysiology of cardiac remodeling.
[Circulation Research]
Dorn Lisa E, Lawrence William R, Petrosino Jennifer, Xu Xianyao, Hund Thomas J, Whitson Bryan A, Stratton Matthew S, Janssen Paul ML, Mohler Peter J, Schlosser Anders, Sørensen Grith Lykke, & Accornero Federica. (n.d.). Microfibrillar-Associated Protein 4 Regulates Stress-Induced Cardiac Remodeling. Circulation Research, 0(0). https://doi.org/10.1161/CIRCRESAHA.120.317146 Cite
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Sarcoplasmic Reticular Ca2+-ATPase Inhibition Paradoxically Upregulates Murine Skeletal Muscle Nav1.4 Function

Loose patch clamping determined Na+ current families in intact native murine gastrocnemius skeletal myocytes, minimising artefactual [Ca2+]i perturbations.
[Scientific Reports]
Liu, S. X., Matthews, H. R., & Huang, C. L.-H. (2021). Sarcoplasmic reticular Ca 2+ -ATPase inhibition paradoxically upregulates murine skeletal muscle Na v 1.4 function. Scientific Reports, 11(1), 2846. https://doi.org/10.1038/s41598-021-82493-w Cite
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FoxP1 Is a Transcriptional Repressor Associated with Cancer Cachexia that Induces Skeletal Muscle Wasting and Weakness

Researchers investigated the biological significance of Forkhead box P1, a transcriptional repressor that they demonstrated is up‐regulated in skeletal muscle in multiple models of cancer cachexia and in cachectic cancer patients.
[Journal of Cachexia Sarcopenia and Muscle]
Neyroud, D., Nosacka, R. L., Callaway, C. S., Trevino, J. G., Hu, H., Judge, S. M., & Judge, A. R. (n.d.). FoxP1 is a transcriptional repressor associated with cancer cachexia that induces skeletal muscle wasting and weakness. Journal of Cachexia, Sarcopenia and Muscle, n/a(n/a). https://doi.org/https://doi.org/10.1002/jcsm.12666 Cite
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Chemical Systems Biology Reveals Mechanisms of Glucocorticoid Receptor Signaling

Researchers used a chemical systems biology approach, ligand class analysis, to examine ligands designed to modulate glucocorticoid receptor activity through distinct structural mechanisms.
[Nature Chemical Biology]
Bruno, N. E., Nwachukwu, J. C., Srinivasan, S., Nettles, C. C., Izard, T., Jin, Z., Nowak, J., Cameron, M. D., Boregowda, S. V., Phinney, D. G., Elemento, O., Liu, X., Ortlund, E. A., Houtman, R., Stavreva, D. A., Hager, G. L., Kamenecka, T. M., Kojetin, D. J., & Nettles, K. W. (2021). Chemical systems biology reveals mechanisms of glucocorticoid receptor signaling. Nature Chemical Biology, 1–10. https://doi.org/10.1038/s41589-020-00719-w Cite
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Pathogenic LMNA Variants Disrupt Cardiac Lamina-Chromatin Interactions and De-Repress Alternative Fate Genes

Researchers introduced LMNA mutations from individuals with dilated cardiomyopathy into human (h)iPSCs and found that hiPSC-derived cardiomyocytes, in contrast to hepatocytes or adipocytes, exhibited aberrant nuclear morphology and specific disruptions in peripheral chromatin.
[Cell Stem Cell]
Shah, P. P., Lv, W., Rhoades, J. H., Poleshko, A., Abbey, D., Caporizzo, M. A., Linares-Saldana, R., Heffler, J. G., Sayed, N., Thomas, D., Wang, Q., Stanton, L. J., Bedi, K., Morley, M. P., Cappola, T. P., Owens, A. T., Margulies, K. B., Frank, D. B., Wu, J. C., … Jain, R. (2021). Pathogenic LMNA variants disrupt cardiac lamina-chromatin interactions and de-repress alternative fate genes. Cell Stem Cell, 0(0). https://doi.org/10.1016/j.stem.2020.12.016 Cite
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Oxidized Phosphatidylcholines Trigger Ferroptosis in Cardiomyocytes during Ischemia/Reperfusion Injury

Cardiomyocyte viability, bioenergetic response and calcium transients were determined in the presence of oxidized phosphatidylcholines (OxPCs). Fragmented OxPCs resulted in a decrease in cell viability with POVPC and PONPC having the most potent cardiotoxic effect in both a concentration and time dependent manner.
[American Journal of Physiology-Heart and Circulatory Physiology]
Stamenkovic, A., O’Hara, K. A., Nelson, D. C., Maddaford, T. G., Edel, A. L., Maddaford, G., Dibrov, E., Aghanoori, M., Kirshenbaum, L. A., Fernyhough, P., Aliani, M., Pierce, G. N., & Ravandi, A. (2021). Oxidized phosphatidylcholines trigger ferroptosis in cardiomyocytes during ischemia/reperfusion injury. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00237.2020 Cite
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