Yuanyuan Shi

Publications97
h-index24
Citations1,949
Highly Influential Citations66
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Valproate protects cells from ER stress-induced lipid accumulation and apoptosis by inhibiting glycogen synthase kinase-3
TLDR
Exposure of HepG2 cells to the branch chain fatty acid, valproate, increases cellular resistance to ER stress-induced dysfunction and it is demonstrated thatvalproate directly inhibits the glycogen synthase kinases (GSK)-3α/β, suggesting GSK3 plays a central role in signaling downstream effects of ER stress.
Tumor necrosis factor α suppresses the mesenchymal stem cell osteogenesis promoter miR‐21 in estrogen deficiency–induced osteoporosis
TLDR
A novel mechanism whereby TNF‐α, suppressing the functional axis of a key miRNA (miR‐21) contributes to estrogen deficiency–induced osteoporosis is identified, which may indicate a molecular basis for novel therapeutic strategies against osteop orosis and other inflammatory bone diseases.
Dose–Response Association Between Physical Activity and Incident Hypertension: A Systematic Review and Meta-Analysis of Cohort Studies
TLDR
This meta-analysis suggests that additional benefits for hypertension prevention occur as the amount of PA increases, and finds no evidence of a nonlinear dose–response association of PA and hypertension.
Evidence supporting a role for endoplasmic reticulum stress in the development of atherosclerosis in a hyperglycaemic mouse model.
TLDR
Dietary supplementation with valproate, a small branched-chain fatty acid that interferes with ER-stress signaling, significantly attenuates accelerated atherogenesis in this model, consistent with a causative role for hyperglycemia-associated ER stress in the development and progression of diabetic atherosclerosis.
Glucosamine-induced endoplasmic reticulum dysfunction is associated with accelerated atherosclerosis in a hyperglycemic mouse model.
TLDR
Using molecular biological and histological techniques, it is shown that hyperglycemia is associated with tissue-specific ER stress, hepatic steatosis, and accelerated atherosclerosis, a novel mechanism that may not only explain how diabetes and hyper glycemia promote atheros sclerosis, but also provide a potential new target for therapeutic intervention.
Hexosamine biosynthesis pathway flux promotes endoplasmic reticulum stress, lipid accumulation, and inflammatory gene expression in hepatic cells.
TLDR
HBP flux-induced ER stress plays a role in the development of hepatic steatosis and atherosclerosis under conditions of hyperglycemia, and hyperglycemic mice presented with elevated markers of hepatics ER stress, glucosamine and lipid accumulation.
Loss of PTEN promotes podocyte cytoskeletal rearrangement, aggravating diabetic nephropathy
TLDR
Results indicate that PTEN is involved in the regulation of cytoskeletal rearrangement in podocytes and that loss of PTEN predisposes to the development of proteinuria and DN.
Metabolic Syndrome and Acute Hyperglycemia Are Associated With Endoplasmic Reticulum Stress in Human Mononuclear Cells
TLDR
There is an association between both acute and chronic dysglycemia and ER stress in humans, and the results indicate that individuals with metabolic syndrome have elevated mRNA levels of genes indicative of ER stress.
Syndecan-2 exerts antifibrotic effects by promoting caveolin-1-mediated transforming growth factor-β receptor I internalization and inhibiting transforming growth factor-β1 signaling.
TLDR
Alveolar macrophage syndecan-2 exerts antifibrotic effects by promoting caveolin-1-dependent TGF-β1 and TβRI internalization and inhibiting TGF -β1 signaling in alveolar epithelial cells, and molecules that facilitate T βRI degradation via endocytosis represent potential therapies for pulmonary fibrosis.
Endoplasmic Reticulum Stress and Glycogen Synthase Kinase-3&bgr; Activation in Apolipoprotein E–Deficient Mouse Models of Accelerated Atherosclerosis
TLDR
Findings support the existence of a common mechanism of accelerated atherosclerosis involving ER stress signaling through activation of GSK3&bgr; and suggest that Atherosclerosis can be attenuated by modulating GSK 3&b gr; phosphorylation.
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