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Nogo-B mediates endothelial oxidative stress and inflammation to promote coronary atherosclerosis in pressure-overloaded mouse hearts.
Redox Biol
December 2023
Department of Physiology and Pathophysiology, School of Basic Medical Sciences, And Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China. Electronic address:
Aims: Endothelial dysfunction plays a pivotal role in atherosclerosis, but the detailed mechanism remains incomplete understood. Nogo-B is an endoplasmic reticulum (ER)-localized protein mediating ER-mitochondrial morphology. We previously showed endothelial Nogo-B as a key regulator of endothelial function in the setting of hypertension.
View Article and Find Full Text PDFAssociation between high serum Nogo-B and hypertension in Chinese Han.
BMC Cardiovasc Disord
June 2022
Department of Cardiology, Dalian Municipal Central Hospital, Dalian, China.
Background: Cellular and animal studies have shown that endoplasmic reticulum protein B (Nogo-B) is associated with hypertension, but that association has not been fully studied in humans. Therefore, the expression levels of Nogo-B were investigated in hypertensive patients.
Methods: The plasma Nogo-B levels of 74 patients with hypertension and 67 non-hypertensive patients were measured by enzyme-linked immunosorbent assay.
Nogo-B promotes angiogenesis and improves cardiac repair after myocardial infarction via activating Notch1 signaling.
Cell Death Dis
April 2022
Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, No. 600. Yi Shan Road, Shanghai, 200233, China.
Nogo-B (Reticulon 4B) is reportedly a regulator of angiogenesis during the development and progression of cancer. However, whether Nogo-B regulates angiogenesis and post-myocardial infarction (MI) cardiac repair remains elusive. In the present study, we aimed to explore the role and underlying mechanisms of Nogo-B in cardiac repair during MI.
View Article and Find Full Text PDFResearch advances on neurite outgrowth inhibitor B receptor.
J Cell Mol Med
July 2020
Department of Neurology, Xiangya Hospital, Central South University, Changsha, China.
Neurite outgrowth inhibitor-B (Nogo-B) is a membrane protein which is extensively expressed in multiple organs, especially in endothelial cells and vascular smooth muscle cells of blood vessels and belongs to the reticulon protein family. Notably, its specific receptor, Nogo-B receptor (NgBR), encoded by NUS1, has been implicated in many crucial cellular processes, such as cholesterol trafficking, lipid metabolism, dolichol synthesis, protein N-glycosylation, vascular remodelling, angiogenesis, tumorigenesis and neurodevelopment. In recent years, accumulating studies have demonstrated the statistically significant changes of NgBR expression levels in human diseases, including Niemann-Pick type C disease, fatty liver, congenital disorders of glycosylation, persistent pulmonary hypertension of the newborn, invasive ductal breast carcinoma, malignant melanoma, non-small cell lung carcinoma, paediatric epilepsy and Parkinson's disease.
View Article and Find Full Text PDFNogo-B Receptor Directs Mitochondria-Associated Membranes to Regulate Vascular Smooth Muscle Cell Proliferation.
Int J Mol Sci
May 2019
Institute of Medicine and Hygienic Equipment for High Altitude Region, College of High Altitude Military Medicine, Army Medical University (Third Military Medical University), Chongqing 400038, China.
Mitochondria-associated membranes (MAM) are a well-recognized contact link between the mitochondria and endoplasmic reticulum that affects mitochondrial biology and vascular smooth muscle cells (VSMCs) proliferation via the regulation of mitochondrial Ca(Ca) influx. Nogo-B receptor (NgBR) plays a vital role in proliferation, epithelial-mesenchymal transition, and chemoresistance of some tumors. Recent studies have revealed that downregulation of NgBR, which stimulates the proliferation of VSMCs, but the underlying mechanism remains unclear.
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