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Endoplasmic Reticulum (ER) Stress-Generated Extracellular Vesicles (Microparticles) Self-Perpetuate ER Stress and Mediate Endothelial Cell Dysfunction Independently of Cell Survival.
(
Frontiers Media
, 2020 , Article)
Circulating extracellular vesicles (EVs) are recognized as biomarkers and effectors of endothelial dysfunction, the initiating step of cardiovascular abnormalities. Among these EVs, microparticles (MPs) are vesicles directly ...
Crosstalk Between Oxidative Stress and Endoplasmic Reticulum (ER) Stress in Endothelial Dysfunction and Aberrant Angiogenesis Associated With Diabetes: A Focus on the Protective Roles of Heme Oxygenase (HO)-1
(
Frontiers Media
, 2019 , Article Review)
Type-2 diabetes prevalence is continuing to rise worldwide due to physical inactivity and obesity epidemic. Diabetes and fluctuations of blood sugar are related to multiple micro- and macrovascular complications, that are ...
Protein Tyrosine Phosphatase (PTP) 1B Inhibition Improves Endoplasmic Reticulum Stress-Induced Apoptosis and Impaired Angiogenic Response in Endothelial Cells
(
Qatar University Press
, 2021 , Poster)
Insulin is not only important for glucose homeostasis, but also plays a critical role in the activation of endothelial nitric oxide synthase (eNOS) to synthesize nitric oxide (NO) and keeping the endothelium functional. ...
Heme oxygenase (HO)-1 induction prevents Endoplasmic Reticulum stress-mediated endothelial cell death and impaired angiogenic capacity
(
Elsevier
, 2016 , Article)
Most of diabetic cardiovascular complications are attributed to endothelial dysfunction and impaired angiogenesis. Endoplasmic Reticulum (ER) and oxidative stresses were shown to play a pivotal role in the development of ...
Temporal cross talk between endoplasmic reticulum and mitochondria regulates oxidative stress and mediates microparticle-induced endothelial dysfunction
(
Mary Ann Liebert, Inc.
, 2017 , Article)
Aims: Circulating microparticles (MPs) from metabolic syndrome patients
and those generated from apoptotic T-cells induce endothelial
dysfunction; however, the molecular and cellular mechanism(s) underlying
in the effects ...