Bo-Wen Wu
Hebei University
5 Papers
Bo-Wen Wu is an academic researcher from Hebei University. The author has contributed to research in topics: Akt/PKB signaling pathway & Synapse. The author has an hindex of 4, co-authored 5 publications.
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Papers
Mesenchymal Stem Cell-Mediated Mitochondrial Transfer: a Therapeutic Approach for Ischemic Stroke.
Meng Lu,Jin-Dong Guo,Bo-Wen Wu,Yu-Hui Zhou,Yu-Hui Zhou,Mi-Shan Wu,Maryam Farzaneh,Seyed Esmaeil Khoshnam +7 more
TL;DR: This review summarizes the research on MSCs-mediated mitochondrial transfer as a therapeutic strategy against ischemic stroke and suggests that mesenchymal stem cells can directly transfer healthy mitochondria to damaged cells, and rescue mitochondrial damage-provoked tissue degeneration.
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Downregulation of microRNA-135b promotes atherosclerotic plaque stabilization in atherosclerotic mice by upregulating erythropoietin receptor
TL;DR: Investigation of the role microRNA‐135b in macrophages and atherosclerotic plaque in mouse models of AS revealed that inhibition of miR‐135B promoted macrophage autophagy and Atherosclerosis plaque stabilization in atherosclerosis mice by inactivating the PI3K/Akt signaling pathway and upregulating EPOR.
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Effects of microRNA-10a on synapse remodeling in hippocampal neurons and neuronal cell proliferation and apoptosis through the BDNF-TrkB signaling pathway in a rat model of Alzheimer's disease.
TL;DR: The results indicated that miR‐10a restrains synapse remodeling and neuronal cell proliferation while promoting apoptosis in AD rats via inhibiting BDNF‐TrkB signaling pathway.
Osteoblast-derived lipocalin-2 regulated by miRNA-96-5p/Foxo1 advances the progression of Alzheimer's disease.
TL;DR: This study shows downregulating miR-96-5p limited AD progression, highlighting miR -96- 5p a potential therapeutic target in treating AD.
SIRT1-mediated deacetylation of NF-κB inhibits the MLCK/MLC2 pathway and the expression of ET-1, thus alleviating the development of coronary artery spasm.
TL;DR: It is suggested that SIRT1 could mediate the deacetylation of NF-κB, disrupt the MLCK/MLC2 pathway and inhibit the expression of ET-1 to relieve CAS, providing a theoretical basis for the prospect of CAS treatment and prevention.