2 results match your criteria: "Shenzhen Research Institute and Li Ka Shing Institute of Health Sciences (W.S.[Affiliation]"
Endothelial TFEB (Transcription Factor EB) Restrains IKK (IκB Kinase)-p65 Pathway to Attenuate Vascular Inflammation in Diabetic db/db Mice.
Arterioscler Thromb Vasc Biol
April 2019
From the Institute of Vascular Medicine, Shenzhen Research Institute and Li Ka Shing Institute of Health Sciences (W.S., C.-L.Z., L.G., L.H., Y.-Y.G., Q.D., L.Z., L.W., X.Y.T., J.-Y.L., Y.H.).
Objective- TFEB (transcription factor EB) was recently reported to be induced by atheroprotective laminar flow and play an anti-atherosclerotic role by inhibiting inflammation in endothelial cells (ECs). This study aims to investigate whether TFEB regulates endothelial inflammation in diabetic db/db mice and the molecular mechanisms involved. Approach and Results- Endothelial denudation shows that TFEB is mainly expressed in ECs in mouse aortas.
View Article and Find Full Text PDFMetformin protects endothelial function in diet-induced obese mice by inhibition of endoplasmic reticulum stress through 5' adenosine monophosphate-activated protein kinase-peroxisome proliferator-activated receptor δ pathway.
Arterioscler Thromb Vasc Biol
April 2014
From Institute of Vascular Medicine, Shenzhen Research Institute, and Li Ka Shing Institute of Health Sciences (W.S.C., X.Y.T., C.W.L., X.Y., Y.H.), and School of Life Sciences (S.S.-T.L., Z.Y.C.), Chinese University of Hong Kong, Hong Kong, China; Department of Cardiovascular Sciences, Houston Methodist Research Institute, Houston, TX (X.Y.T., W.T.W.); and Cardiovascular Research Center, Xi'an Jiaotong University, Xi'an, China (N.W.).
Objective: 5' Adenosine monophosphate-activated protein kinase (AMPK) interacts with peroxisome proliferator-activated receptor δ (PPARδ) to induce gene expression synergistically, whereas the activation of AMPK inhibits endoplasmic reticulum (ER) stress. Whether the vascular benefits of antidiabetic drug metformin (AMPK activator) in diabetes mellitus and obesity is mediated by PPARδ remains unknown. We aim to investigate whether PPARδ is crucial for metformin in ameliorating ER stress and endothelial dysfunction induced by high-fat diet.
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