Zobrazeno 1 - 10
of 21
pro vyhledávání: '"Xiang-tao Zheng"'
Autor:
Kui Chen, Hao-jie Jin, Zi-heng Wu, Bao-fu Zhang, Jun Wu, Zi-yi Huang, Ying-peng Huang, Xin-wu Lu, Xiang-tao Zheng
Publikováno v:
Molecular Medicine, Vol 30, Iss 1, Pp 1-13 (2024)
Abstract Background Vascular calcification (VC) is a complication in diabetes mellitus (DM) patients. Osteogenic phenotype switching of vascular smooth muscle cells (VSMCs) plays a critical role in diabetes-related VC. Mitophagy can inhibit phenotype
Externí odkaz:
https://doaj.org/article/671dcee356c64e7a96f827e21f67e967
Publikováno v:
Molecular Therapy: Nucleic Acids, Vol 20, Iss , Pp 62-72 (2020)
Inflammation and proliferation of vascular smooth muscle cells (VSMCs) are the key events in intimal hyperplasia. This study aimed to explore the mechanism by which long non-coding RNA (lncRNA) KCNQ1OT1 affects VSMC inflammation and proliferation in
Externí odkaz:
https://doaj.org/article/ea067fdb4d6a472f8d1fb85bca81f3a2
Publikováno v:
SAGE Open Medical Case Reports, Vol 3 (2015)
Objective: Acute common iliac artery occlusion which results from blunt abdominal trauma is rare and potentially leads to a late diagnosis. Methods: We report a case of a 58-year-old patient who suffered a late diagnosed acute left common iliac arter
Externí odkaz:
https://doaj.org/article/d6c9daf552524520b25f46aeae3e580a
Autor:
Yu-Ming Wang, Fang-Chen Gong, Xing Qi, Yan-Jun Zheng, Xiang-Tao Zheng, Ying Chen, Zhi-Tao Yang, null Qing-Ye, En-Qiang Mao, Er-Zhen Chen
Publikováno v:
Oxidative Medicine and Cellular Longevity. 2022:1-29
Background. Ferroptosis is a nonapoptotic form of programmed cell death, which may be related to the occurrence and development of sepsis-induced acute respiratory distress syndrome (ARDS)/acute lung injury (ALI). Mucin 1 (MUC1) is a kind of macromol
Autor:
Bao-fu Zhang, Zi-heng Wu, Jie Deng, Hao-jie Jin, Wei-biao Chen, Sai Zhang, Xiu-jie Liu, Wan-tie Wang, Xiang-tao Zheng
Publikováno v:
Biological Chemistry. 403:317-329
Abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by insulin resistance facilitates intimal hyperplasia of type 2 diabetes mellitus (T2DM) and N6-methyladenosine (m6A) methylation modification mediates the VSMC proliferation. Thi
Autor:
Bao-Fu, Zhang, Zi-Heng, Wu, Jie, Deng, Hao-Jie, Jin, Wei-Biao, Chen, Sai, Zhang, Xiu-Jie, Liu, Wan-Tie, Wang, Xiang-Tao, Zheng
Publikováno v:
Biological chemistryReferences. 403(3)
Abnormal proliferation of vascular smooth muscle cells (VSMCs) induced by insulin resistance facilitates intimal hyperplasia of type 2 diabetes mellitus (T2DM) and N6-methyladenosine (m
Autor:
Yan-Jun, Zheng, Xiao-Juan, Zhu, Yu-Wei, Chen, Yu-Zhen, Zheng, Yi, Zhou, Wen-Jie, Chen, Xiang-Tao, Zheng, Ming, Zhong, Zhi-Tao, Yang, En-Qiang, Mao, Er-Zhen, Chen, Ying, Chen
Publikováno v:
Annals of Translational Medicine. 10:781-781
Existing scoring systems have limitations in predicting the in-hospital mortality of adult sepsis patients. We aimed to develop and validate a novel risk score for predicting the in-hospital mortality of adult sepsis patients.The clinical data of 1,3
Publikováno v:
Cell Adhesion & Migration
Cell Adhesion & Migration, Vol 13, Iss 1, Pp 41-49 (2019)
Cell Adhesion & Migration, Vol 13, Iss 1, Pp 41-49 (2019)
In this study, we investigated the role ofhistone deacetylase 4 (HDAC4) and MEG3/miR-125a-5p/interferonregulatoryfactor 1 (IRF1) on vascular smooth muscle cell (VSMCs)proliferation. Platelet derived growth factor (PDGF)-BB was used toinduce the proli
Publikováno v:
Molecular Therapy. Nucleic Acids
Molecular Therapy: Nucleic Acids, Vol 20, Iss, Pp 62-72 (2020)
Molecular Therapy: Nucleic Acids, Vol 20, Iss, Pp 62-72 (2020)
Inflammation and proliferation of vascular smooth muscle cells (VSMCs) are the key events in intimal hyperplasia. This study aimed to explore the mechanism by which long non-coding RNA (lncRNA) KCNQ1OT1 affects VSMC inflammation and proliferation in
Publikováno v:
Molecular and Cellular Biochemistry. 425:125-138
Vascular endothelial cells are highly sensitive to oxidative stress, and this is one of the mechanisms by which widespread endothelial dysfunction is induced in most cardiovascular diseases and disorders. However, how these cells can survive in oxida