title: Role of endoplasmic reticulum stress signalling in diabetic endothelial dysfunction and atherosclerosis.
abstract: It is well established that diabetes mellitus accelerates atherosclerotic vascular disease. Endothelial injury has been proposed to be the initial event in the pathogenesis of atherosclerosis. Endothelium not only acts as a semi-selective barrier but also serves physiological and metabolic functions. Diabetes or high glucose in circulation triggers a series of intracellular responses and organ damage such as endothelial dysfunction and apoptosis. One such response is high glucose-induced chronic endoplasmic reticulum stress in the endothelium. The unfolded protein response is an acute reaction that enables cells to overcome endoplasmic reticulum stress. However, when chronically persistent, endoplasmic reticulum stress response could ultimately lead to endothelial dysfunction and atherosclerosis. Herein, we discuss the scientific advances in understanding endoplasmic reticulum stress-induced endothelial dysfunction, the pathogenesis of diabetes-accelerated atherosclerosis and endoplasmic reticulum stress as a potential target in therapies for diabetic atherosclerosis.
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Yunzhou
authors.initials: Y
authors.lastname: Dong
authors.affiliation: Department of Biosciences, Rice University, Houston, TX, USA.
authors.forename: Conrad
authors.initials: C
authors.lastname: Fernandes
authors.affiliation: Department of Internal Medicine, Charles R. Drew University of Medicine and Science, University of California-Los Angeles School of Medicine, Los Angeles, CA, USA.
authors.forename: Yanjun
authors.initials: Y
authors.lastname: Liu
authors.affiliation: Department of Internal Medicine, Charles R. Drew University of Medicine and Science, University of California-Los Angeles School of Medicine, Los Angeles, CA, USA.
authors.forename: Yong
authors.initials: Y
authors.lastname: Wu
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Hao
authors.initials: H
authors.lastname: Wu
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Megan L
authors.initials: ML
authors.lastname: Brophy
authors.affiliation: Department of Biological Chemistry & Molecular Pharmacology, Harvard Medical School, Boston, MA, USA.
authors.forename: Lin
authors.initials: L
authors.lastname: Deng
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Kai
authors.initials: K
authors.lastname: Song
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Aiyun
authors.initials: A
authors.lastname: Wen
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA.
authors.forename: Scott
authors.initials: S
authors.lastname: Wong
authors.affiliation: Department of Biology, Jinan University, Guangzhou, China.
authors.forename: Daoguang
authors.initials: D
authors.lastname: Yan
authors.affiliation: Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation, Oklahoma, OK, USA.
authors.forename: Rheal
authors.initials: R
authors.lastname: Towner
authors.affiliation: Vascular Biology Program, Department of Surgery, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA hong.chen@childrens.harvard.edu.
authors.forename: Hong
authors.initials: H
authors.lastname: Chen
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000627:therapeutic use; D003925:Diabetic Angiopathies / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D004721:Endoplasmic Reticulum / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D058226:Plaque, Atherosclerotic; D015398:Signal Transduction
chemical_list: D002317:Cardiovascular Agents
keywords: Diabetes mellitus; atherosclerosis; endoplasmic reticulum stress; endothelial dysfunction