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Total 34 results found since Jan 2013.

Linc00657 promoted pyroptosis in THP-1-derived macrophages and exacerbated atherosclerosis via the miR-106b-5p/TXNIP/NLRP3 axis
This study was designed to investigate the effects and underlying mechanisms of linc00657 in atherogenesis. The results showed that ox-LDL treatment significantly induced pyroptosis in human THP-1-derived macrophages. The secretion levels of LDH and pro-inflammatory factors were markedly enhanced, and the integrity of plasma membranes was disrupted in ox-LDL-treated THP-1-derived macrophages. These effects were significantly compensated after transfection with linc00657 siRNA and became more evident by linc00657 overexpression. Moreover, the effects of linc00657 overexpression on pyroptosis of THP-1-derived macrophages can...
Source: Atherosclerosis - September 21, 2023 Category: Cardiology Authors: Yin Liang Xiao-Dan Xu Xi Xu Yang-Bo Cai Zi-Xian Zhu Lin Zhu Kun Ren Source Type: research

TRIM65 Suppresses oxLDL-induced Endothelial Inflammation by Interaction with VCAM-1 in Atherogenesis
CONCLUSION: Our studies indicate that TRIM65 attenuates the endothelial inflammatory response by targeting VCAM-1 for ubiquitination and provides a potential therapeutic target for the inhibition of endothelial inflammation in AS.PMID:37608612 | DOI:10.2174/0929867331666230822152350
Source: Atherosclerosis - August 23, 2023 Category: Cardiology Authors: Xiao-Feng Ma Yi-Ren Zhou Zhi-Xiang Zhou Hui-Ting Liu Bo-Bin Zhoua Nian-Hua Deng Kun Zhou Zhen Tian Ze-Fan Wu Xi-Yan Liu Ming-Gui Fu Zhi-Sheng Jiang Source Type: research

GP73 enhances the ox-LDL-induced inflammatory response in THP-1 derived macrophages via affecting NLRP3 inflammasome signaling
CONCLUSIONS: We demonstrated that GP73 promoted the ox-LDL-induced inflammation in macrophages by affecting the NF-κB/NLRP3 inflammasome signaling, and may play a role in atherosclerosis.PMID:37271284 | DOI:10.1016/j.ijcard.2023.05.059
Source: Atherosclerosis - June 4, 2023 Category: Cardiology Authors: Yi-Fen Lin Miao-Hong Li Ri-Hua Huang Shao-Zhao Zhang Xing-Feng Xu Hui-Min Zhou Meng-Hui Liu Xin-Xue Liao Li-Zhen Liao Yue Guo Xiao-Dong Zhuang Source Type: research

Endothelial PHACTR1 Promotes Endothelial Activation and Atherosclerosis by Repressing PPAR γ Activity Under Disturbed Flow in Mice
CONCLUSIONS: Our results identified endothelial PHACTR1 as a novel PPARγ corepressor to promote atherosclerosis in disturbed flow regions. Endothelial PHACTR1 is a potential therapeutic target for atherosclerosis treatment.PMID:37199156 | DOI:10.1161/ATVBAHA.122.318173
Source: Atherosclerosis - May 18, 2023 Category: Cardiology Authors: Dongyang Jiang Hao Liu Guofu Zhu Xiankai Li Linlin Fan Faxue Zhao Chong Xu Shumin Wang Yara Rose Jordan Rhen Ze Yu Yiheng Yin Yuling Gu Xiangbin Xu Edward A Fisher Junbo Ge Yawei Xu Jinjiang Pang Source Type: research

Diabetes is accompanied by secretion of pro-atherosclerotic exosomes from vascular smooth muscle cells
CONCLUSION: These data identify a novel paracrine signaling pathway that promotes the cardiovascular complications of diabetes mellitus.PMID:37179303 | DOI:10.1186/s12933-023-01833-4
Source: Atherosclerosis - May 13, 2023 Category: Cardiology Authors: Heng Yu Hunter F Douglas Donald Wathieu Ryan A Braun Christine Edomwande Daniel J Lightell Thaidan Pham Natasha C Klingenberg Shelia Pugh Bishop Damir B Khismatullin T Cooper Woods Source Type: research

Excessive exogenous cholesterol activating intestinal LXR α-ABCA1/G5/G8 signaling pathway can not reverse atherosclerosis in ApoE < sup > -/- < /sup > mice
CONCLUSION: In a high-cholesterol environment, the intestine promotes the excretion of cholesterol from the cell through the LXRα-ABCA1/G5/G8 pathway, reduces the intestinal intake of a variety of exogenous cholesterol, and reduces the risk of AS.PMID:37061692 | DOI:10.1186/s12944-023-01810-6
Source: Atherosclerosis - April 15, 2023 Category: Cardiology Authors: Xichao Yu Xue Ding Han Feng Yunhui Bi Yu Li Jinjun Shan Huimin Bian Source Type: research

Circulating Extracellular Vesicle-Propagated microRNA Signature as a Vascular Calcification Factor in Chronic Kidney Disease
CONCLUSIONS: The miRNA transcriptomic signature of circulating sEVs uncovered their pathologic role, devoid of the calcification-protective miRNAs that target VEGFA signaling in CKD-driven vascular calcification. These sEV-propagated miRNAs are potential biomarkers and therapeutic targets for vascular calcification.PMID:36700539 | DOI:10.1161/CIRCRESAHA.122.321939
Source: Atherosclerosis - January 26, 2023 Category: Cardiology Authors: Takaaki Koide Shintaro Mandai Reo Kitaoka Hisazumi Matsuki Motoko Chiga Kouhei Yamamoto Kotaro Yoshioka Yohsuke Yagi Soichiro Suzuki Tamami Fujiki Fumiaki Ando Takayasu Mori Koichiro Susa Soichiro Iimori Shotaro Naito Eisei Sohara Tatemitsu Rai Takanori Y Source Type: research

SRC-3 deficiency prevents atherosclerosis development by decreasing endothelial ICAM-1 expression to attenuate macrophage recruitment
In this study, we found that SRC-3-/-ApoE-/- mice have reduced atherosclerotic lesions and necrotic areas in their aortas and aortic roots compared with SRC-3+/+ApoE-/- mice after Western diet (WD) feeding for 12 weeks. RNA-Seq and Western blot analyses of the aorta revealed that SRC-3 was required for maintaining the expression of ICAM-1, which was required for macrophage recruitment and atherosclerosis development. siRNA-mediated knockdown of SRC-3 in endothelial cells significantly reduced WD-induced atherosclerotic plaque formation. Additionally, treatment of ApoE-/- mice with SRC-3 inhibitor bufalin prevented atherosc...
Source: Atherosclerosis - October 20, 2022 Category: Cardiology Authors: Wenbo Chen Wuyang Zheng Shixiao Liu Qiang Su Kangxi Ding Ziguan Zhang Ping Luo Yong Zhang Jianming Xu Chundong Yu Weihua Li Zhengrong Huang Source Type: research

Cardiac Alarmins as Residual Risk Markers of Atherosclerosis under Hypolipidemic Therapy
Int J Mol Sci. 2022 Sep 22;23(19):11174. doi: 10.3390/ijms231911174.ABSTRACTIncreased levels of low-density lipoproteins are the main risk factor in the initiation and progression of atherosclerosis. Although statin treatment can effectively lower these levels, there is still a residual risk of cardiovascular events. We hypothesize that a specific panel of stress-sensing molecules (alarmins) could indicate the persistence of silent atherosclerosis residual risk. New Zealand White rabbits were divided into: control group (C), a group that received a high-fat diet for twelve weeks (Au), and a treated hyperlipidemic group wit...
Source: Atherosclerosis - October 14, 2022 Category: Cardiology Authors: Viorel I Suica Elena Uyy Luminita Ivan Raluca M Boteanu Aurel Cerveanu-Hogas Rune Hansen Felicia Antohe Source Type: research

miR-351 promotes atherosclerosis in diabetes by inhibiting the ITGB3/PIK3R1/Akt pathway and induces endothelial cell injury and lipid accumulation
CONCLUSION: Silencing miR-351 upregulates ITGB3 and activates the PIK3R1/Akt pathway, thereby exerting anti-apoptosis and protective effects on endothelial cells.PMID:36180828 | DOI:10.1186/s10020-022-00547-9
Source: Atherosclerosis - September 30, 2022 Category: Cardiology Authors: Hong Li Dan Song Qihui Liu Linlin Li Xiaoshi Sun Jiamei Guo Dianlian Li Ping Li Source Type: research

Sphingosine 1-phosphate receptor 2 promotes erythrocyte clearance by vascular smooth muscle cells in intraplaque hemorrhage through MFG-E8 production
Cell Signal. 2022 Jul 26:110419. doi: 10.1016/j.cellsig.2022.110419. Online ahead of print.ABSTRACTIntraplaque hemorrhage (IPH) accelerates atherosclerosis progression. To scavenge excessive red blood cells (RBCs), vascular smooth muscle cells (VSMCs) with great plasticity may function as phagocytes. Here, we investigated the erythrophagocytosis function of VSMCs and possible regulations involved. Based on transcriptional microarray analysis, Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis showed that genes up-regulated in human carotid atheroma with IPH were enriched in functions of phagocytic activiti...
Source: Atherosclerosis - July 29, 2022 Category: Cardiology Authors: Daorong Pan Wen Wu Guangfeng Zuo Xiangrong Xie Hui Li Xiaomin Ren Chaohua Kong Wenying Zhou Zihan Zhang Martin Waterfall Shaoliang Chen Source Type: research