Scientists discuss recent progress regarding the identification of unknown hypermethylated genes in colon cancers and IBD, as well as their possible role in clinical practice, which will have important clinical significance, particularly in the era of the personalized medicine.
Indoxyl sulfate provoked muscular strength loss, reactive oxygen species (ROS) generation, and mitochondrial impairment. Although the β2-AR agonist could increase the muscular mass with ROS reduction, development of therapeutic interventions for restoring skeletal muscle function is still awaited.
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The authors compare the mechanisms by which fibroblasts control local immune responses, as well as the factors regulating their inflammatory and suppressive profiles, in different tissues and pathological settings.
[Nature Reviews Immunology]
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Researchers identified microRNA-146a as a major negative regulator of colonic inflammation and associated tumorigenesis by modulating IL-17 responses.
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Garo, L. P., Ajay, A. K., Fujiwara, M., Gabriely, G., Raheja, R., Kuhn, C., Kenyon, B., Skillin, N., Kadowaki-Saga, R., Saxena, S., & Murugaiyan, G. (2021). MicroRNA-146a limits tumorigenic inflammation in colorectal cancer. Nature Communications, 12(1), 2419. https://doi.org/10.1038/s41467-021-22641-y Cite
Scientists explored the effect of M2a macrophages on the development of benign prostatic hyperplasia via insulin-like growth factor 1.
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Qian, Q., He, W., Liu, D., Yin, J., Ye, L., Chen, P., Xu, D., Liu, J., Li, Y., Zeng, G., Li, M., Wu, Z., Zhang, Y., Wang, X., DiSanto, M. E., & Zhang, X. (n.d.). M2a macrophage can rescue proliferation and gene expression of benign prostate hyperplasia epithelial and stroma cells from insulin-like growth factor 1 knockdown. The Prostate, n/a(n/a). https://doi.org/https://doi.org/10.1002/pros.24131 Cite
Scientists found that that Golgi membrane protein 1 (GOLM1) suppressed colorectal tumorigenesis via maintenance of intestinal epithelial barrier.
[Signal Transduction and Targeted Therapy]
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Pu, Y., Song, Y., Zhang, M., Long, C., Li, J., Wang, Y., Xu, Y., Pan, F., Zhao, N., Zhang, X., Xu, Y., Cui, J., Wang, H., Li, Y., Zhao, Y., Jin, D., & Zhang, H. (2021). GOLM1 restricts colitis and colon tumorigenesis by ensuring Notch signaling equilibrium in intestinal homeostasis. Signal Transduction and Targeted Therapy, 6(1), 1–15. https://doi.org/10.1038/s41392-021-00535-1 Cite
Investigators focus on the role of NLRP3 inflammasome and its components in breast cancer signaling, highlighting that a more detailed understanding of the clinical relevance of these pathways could significantly contribute to the development of novel therapeutic strategies for breast cancer.
[Journal of Biomedical Science]
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Faria, S. S., Costantini, S., de Lima, V. C. C., de Andrade, V. P., Rialland, M., Cedric, R., Budillon, A., & Magalhães, K. G. (2021). NLRP3 inflammasome-mediated cytokine production and pyroptosis cell death in breast cancer. Journal of Biomedical Science, 28(1), 26. https://doi.org/10.1186/s12929-021-00724-8 Cite
Scientists discuss a paradigm shift by suggesting that beyond these reactions, chronic inflammation is driven by imprinted, pathogenic ‘memory’ cells of the immune system.
[Nature Reviews Rheumatology]
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Both global and endothelial cell-specific inducible knockout of bone morphogenetic protein-binding endothelial regulator cause hyperinsulinemia, glucose intolerance and insulin resistance without increasing inflammation in metabolic tissues in mice.
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Researchers optimized fibroblasts derived from iPS cell matrix production by boosting matrix deposition, without affecting its composition.
[Journal of Biomedical Materials Research Part A]
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Marinkovic, M., Sridharan, R., Santarella, F., Smith, A., Garlick, J. A., & Kearney, C. J. (n.d.). Optimization of extracellular matrix production from human induced pluripotent stem cell-derived fibroblasts for scaffold fabrication for application in wound healing. Journal of Biomedical Materials Research Part A, n/a(n/a). https://doi.org/https://doi.org/10.1002/jbm.a.37173 Cite
The authors provided novel spatiotemporal evidence that myelin and cytosolic phospholipase-A2 (cPLA2) played an important role in the pathophysiology of spinal cord injury inflammation and the phenotype-specific response to myelin implicate diverse roles of myelin in neuroinflammatory conditions.
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