Glial Cells in the Driver Seat of Leukodystrophy Pathogenesis

The authors take a closer look at multiple leukodystrophies, classified based on the primary glial cell type that is affected.
[Neurobiology of Disease]
Garcia, L., Hacker, J. L., Sase, S., Adang, L., & Almad, A. (2020). Glial cells in the driver seat of leukodystrophy pathogenesis. Neurobiology of Disease, 105087. https://doi.org/10.1016/j.nbd.2020.105087 Cite
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Dietary Docosahexaenoic Acid Inhibits Neurodegeneration and Prevents Stroke

Reviewers describe the effects of dietary docosahexaenoic acid on ischemic stroke‐associated neuronal damage and its role in stroke prevention.
[Journal of Neuroscience Research]
Yamagata, K. (n.d.). Dietary docosahexaenoic acid inhibits neurodegeneration and prevents stroke. Journal of Neuroscience Research, n/a(n/a). https://doi.org/10.1002/jnr.24728 Cite
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Why Do Intestinal Epithelial Cells Express MHC Class II?

Recent studies investigating the role of MHC class II+ exosomes released by Intestinal epithelial cells report conflicting findings of either immune enhancing or immunosuppressive activities. In addition to modulating inflammatory responses, recent findings suggest that MHC class II expression by intestinal stem cells may elicit crosstalk that promotes epithelial renewal.
[Immunology]
Heuberger, C., Pott, J., & Maloy, K. J. (n.d.). Why do Intestinal Epithelial Cells Express MHC Class II? Immunology, n/a(n/a). https://doi.org/10.1111/imm.13270 Cite
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Critical Role of HOX Transcript Antisense Intergenic RNA (HOTAIR) in Gliomas

The authors provide evidence on the functional role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas and discuss the benefits of its targeting as a novel approach toward glioma treatment.
[Journal of Molecular Medicine-Jmm]
Angelopoulou, E., Paudel, Y. N., & Piperi, C. (2020). Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas. Journal of Molecular Medicine. https://doi.org/10.1007/s00109-020-01984-x Cite
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Understanding Lipotoxicity in NAFLD Pathogenesis: Is CD36 a Key Driver?

Investigators provide succinct insights into the molecular mechanisms responsible for lipotoxicity in non-alcoholic fatty liver disease (NAFLD), including ER and oxidative stress, autophagy, lipoapotosis and inflammation. They highlight the role of CD36/FAT fatty acid translocase in NAFLD pathogenesis.
[Cell Death & Disease]
Rada, P., González-Rodríguez, Á., García-Monzón, C., & Valverde, Á. M. (2020). Understanding lipotoxicity in NAFLD pathogenesis: is CD36 a key driver? Cell Death & Disease, 11(9), 1–15. https://doi.org/10.1038/s41419-020-03003-w Cite
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WNT–β-Catenin Signaling – A Versatile Player in Kidney Injury and Repair

WNT–β-catenin signaling is involved in chronic kidney disease-associated vascular calcification and mineral bone disease. The WNT–β-catenin pathway is tightly regulated, for example, by proteins of the Dickkopf family.
[Nature Reviews Nephrology]
Schunk, S. J., Floege, J., Fliser, D., & Speer, T. (2020). WNT–β-catenin signalling — a versatile player in kidney injury and repair. Nature Reviews Nephrology, 1–13. https://doi.org/10.1038/s41581-020-00343-w Cite
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Neurological Complications Associated with the Blood-Brain Barrier Damage Induced by the Inflammatory Response during SARS-CoV-2 Infection

Scientists analyze and described the possible mechanisms causative of brain injury after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. They propose that potential routes of SARS-CoV-2 neuro-invasion are determinant factors in the process.
[Molecular Neurobiology]
Alquisiras-Burgos, I., Peralta-Arrieta, I., Alonso-Palomares, L. A., Zacapala-Gómez, A. E., Salmerón-Bárcenas, E. G., & Aguilera, P. (2020). Neurological Complications Associated with the Blood-Brain Barrier Damage Induced by the Inflammatory Response During SARS-CoV-2 Infection. Molecular Neurobiology. https://doi.org/10.1007/s12035-020-02134-7 Cite
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Autophagy and Cardiac Diseases: Therapeutic Potential of Natural Products

The authors focus on the role of autophagy in various cardiac diseases and the pharmacological basis and therapeutic potential of reported natural products in cardiac diseases by modifying autophagic processes.
[Medicinal Research Reviews]
Wu, X., Liu, Z., Yu, X.-Y., Xu, S., & Luo, J. (n.d.). Autophagy and cardiac diseases: Therapeutic potential of natural products. Medicinal Research Reviews, n/a(n/a). https://doi.org/10.1002/med.21733 Cite
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Translational Neuroendocrinology of Human Skin: Concepts and Perspectives

The authors focus on how neurohormones impact human skin physiology and pathology. They highlight basic concepts, major open questions, and translational research perspectives in cutaneous neuroendocrinology and argue that greater emphasis on neuroendocrine human skin research will foster the development of novel dermatological therapies.
[Trends in Molecular Medicine]
Ramot, Y., Böhm, M., & Paus, R. (2020). Translational Neuroendocrinology of Human Skin: Concepts and Perspectives. Trends in Molecular Medicine, 0(0). https://doi.org/10.1016/j.molmed.2020.09.002 Cite
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Cellular Heterogeneity and Microenvironmental Control of Skin Cancer

In this review, focusing on the skin, scientists investigate potential key mechanisms that ensure tissue homeostasis despite the presence of mutant cells, as well as critical factors that may nudge the balance from homeostasis to tumor formation.
[Journal of Internal Medicine]
Lichtenberger, B. M., & Kasper, M. (n.d.). Cellular heterogeneity and microenvironmental control of skin cancer. Journal of Internal Medicine, n/a(n/a). https://doi.org/10.1111/joim.13177 Cite
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Cell Senescence, Multiple Organelle Dysfunction and Atherosclerosis

The authors present an objective review of the key senescence-related alterations of the major intracellular organelles and analyze the role of relevant cell types for senescence and atherogenesis.
[Cells]
Machado-Oliveira, G., Ramos, C., Marques, A. R. A., & Vieira, O. V. (2020). Cell Senescence, Multiple Organelle Dysfunction and Atherosclerosis. Cells, 9(10), 2146. https://doi.org/10.3390/cells9102146 Cite
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