Hif-1a Suppresses ROS-Induced Proliferation of Cardiac Fibroblasts Following Myocardial Infarction

Investigators reported that cardiac fibroblasts and mesenchymal progenitors are more hypoxic than other cardiac interstitial populations, express more hypoxia-inducible factor 1α (HIF-1α), and exhibited increased glycolytic metabolism.
[Cell Stem Cell]
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MicroRNAs and Angiogenesis: A New Era for the Management of Colorectal Cancer

Scientists describe the latest advances in the understanding of miRNAs and their corresponding targets that play a role in colorectal cancer angiogenesis and discuss possible miRNA-based therapeutic strategies.
[Cancer Cell International]
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Dual Effects of Hypoxia on Proliferation and Osteogenic Differentiation of Mouse Clonal Mesenchymal Stem Cells

Mouse clonal MSCs were cultured on a Cytodex 3 microcarrier in a spinner flask for a suspension culture under hypoxia condition to increase mass productivity.
[Bioprocess and Biosystems Engineering]
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Allogeneic Human Umbilical Cord Wharton’s Jelly Stem Cells Increase Several-Fold the Expansion of Human Cord Blood CD34+ Cells Both In Vitro and In Vivo

Scientists performed an in-depth evaluation of the primitiveness, migration, adhesion, maturation, mitochondrial behavior, and pathway mechanisms of this platform using conventional assays followed by the evaluation of engraftment potential of the expanded CD34+ cells in an in vivo murine model.
[Stem Cell Research & Therapy]
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The Importance of Hypoxia-Inducible Factors (HIF-1 and HIF-2) for the Pathophysiology of Inflammatory Bowel Disease

Myeloid hypoxia inducible factors(HIF)-1α and HIF-2α played opposing roles in acute dextran sodium sulfate colitis. Thus, not only a cell type specific, but also the isoform specific modulation of HIFs needs to be addressed in attempts to modify HIF for therapeutic purposes.
[International Journal of Molecular Sciences]
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Macrophage Metabolic Reprogramming Presents a Therapeutic Target in Lupus Nephritis

Investigators found that human and mouse macrophages underwent a switch to glycolysis in response to IgG immune complex stimulation, mirroring macrophage metabolic changes in inflamed tissue in vivo. This metabolic reprogramming was required to generate a number of proinflammatory mediators, including IL-1β, and was dependent on mTOR and hypoxia-inducible factor-1α.
[Proceedings of the National Academy of Sciences of the United States of America]
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