NR3C2 mediates oxidised low-density lipoprotein-induced human coronary endothelial cells dysfunction via modulation of NLRP3 inflammasome activation

Chen, Xiaofan; Li, Weidong; Chang, Chengdong

doi:10.1080/08916934.2023.2189135

Cited by 9 publications

(3 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…By contrast, NR3C2 silencing inhibited ox-LDL-induced inflammation and apoptosis in these cells. The aforementioned study supported the significant role of NR3C2 and NLRP3 in ox-LDL-induced inflammation in HCAECs and further highlighted their values in the inflammatory response in CAD [41]. NLRP3 activation in macrophages is a critical mechanism driving atherosclerotic inflammation, which ultimately leads to the development of atherosclerosis [42,43].…”

Section: Nlrp3 Inflammasome and Atherosclerosissupporting

confidence: 65%

Inflammatory Mediators of Endothelial Dysfunction

Dri

Lampas

Lazaros

et al. 2023

Life

View full text Add to dashboard Cite

Endothelial dysfunction (ED) is characterized by imbalanced vasodilation and vasoconstriction, elevated reactive oxygen species (ROS), and inflammatory factors, as well as deficiency of nitric oxide (NO) bioavailability. It has been reported that the maintenance of endothelial cell integrity serves a significant role in human health and disease due to the involvement of the endothelium in several processes, such as regulation of vascular tone, regulation of hemostasis and thrombosis, cell adhesion, smooth muscle cell proliferation, and vascular inflammation. Inflammatory modulators/biomarkers, such as IL-1α, IL-1β, IL-6, IL-12, IL-15, IL-18, and tumor necrosis factor α, or alternative anti-inflammatory cytokine IL-10, and adhesion molecules (ICAM-1, VCAM-1), involved in atherosclerosis progression have been shown to predict cardiovascular diseases. Furthermore, several signaling pathways, such as NLRP3 inflammasome, that are associated with the inflammatory response and the disrupted H2S bioavailability are postulated to be new indicators for endothelial cell inflammation and its associated endothelial dysfunction. In this review, we summarize the knowledge of a plethora of reviews, research articles, and clinical trials concerning the key inflammatory modulators and signaling pathways in atherosclerosis due to endothelial dysfunction.

show abstract

Section: Nlrp3 Inflammasome and Atherosclerosissupporting

confidence: 65%

Inflammatory Mediators of Endothelial Dysfunction

Dri

Lampas

Lazaros

et al. 2023

Life

View full text Add to dashboard Cite

show abstract

“…The related mechanism of NR3C2 has been reported. In ox-LDL-induced human coronary endothelial cells, transcription of NR3C2 promotes NLRP3 expression ( 22 ). The inhibition of proliferation and induction of cell cycle arrest in colorectal cancer cells was observed with NR3C2 ( 23 ).…”

Section: Discussionmentioning

confidence: 99%

Validation of prognostic signature and exploring the immune-related mechanisms for NR3C2 in clear cell renal cell carcinoma

Chen,

Yin,

Chen

et al. 2023

Transl Cancer Res

View full text Add to dashboard Cite

Background Previous studies have verified that NR3C2 inhibits tumor cell proliferation, invasion, and migration. However, there is a lack of independent validation cohorts for verifying the prognostic value of NR3C2 in clear cell renal cell carcinoma (ccRCC), and its underlying antitumor mechanisms remain unclear. Methods We first obtained dates from the online public databases. Then R language or online public database was used for bioinformatics analyses to evaluate the effect of NR3C2 on the diagnosis, prognosis, and immune microenvironment in ccRCC patients. Finally, the results were verified by our own cohort and immunofluorescence (IF) staining. Results The present study yielded significant findings regarding the expression of NR3C2 in ccRCC compared to control tissues. Specifically, NR3C2 expression was found to be significantly reduced in ccRCC and was observed to be correlated with tumor stage. Additionally, patients with lower NR3C2 expression exhibited shorter overall survival (OS), disease-specific survival, and progress-free survival. Univariable and multivariate Cox analyses further identified NR3C2 expression as an independent prognostic factor for ccRCC. Receiver operating characteristic (ROC) analysis demonstrated that NR3C2 was a highly accurate marker for distinguishing tumors from normal kidney tissue, with an area under the curve (AUC) of 0.959. Further analyses using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis suggested that NR3C2 may play a role in various biological processes and pathways related to tumor immune microenvironment (TIM). The expression of NR3C2 exhibited significant positive correlations with the levels of infiltration of CD4 + and CD8 + T cells, as well as an association with immune checkpoints. Conclusions Our exploratory study suggested that NR3C2 could serve as a novel biomarker for predicting survival in patients with ccRCC and the molecular mechanisms owe partly to immune cell infiltration.

show abstract

“…The molecular mechanisms underlying endothelial dysfunction are complex and influenced by a multitude of pathological stimuli, including NO, low‐density lipoprotein (LDL), reactive oxygen species (ROS), shear stress, and high glucose. 11 , 12 , 13 , 14 , 15 Although many researches regarding endothelial dysfunction have been studied, there still remains a deficiency in diagnostic and therapeutic strategies for endothelial dysfunction‐related diseases. Further elucidation of the molecular mechanisms governing endothelial dysfunction holds promise for advancing its clinical management.…”

Section: Introductionmentioning

confidence: 99%

Endothelial dysfunction: molecular mechanisms and clinical implications

Wang,

2024

MedComm

View full text Add to dashboard Cite

Cardiovascular disease (CVD) and its complications are a leading cause of death worldwide. Endothelial dysfunction plays a crucial role in the initiation and progression of CVD, serving as a pivotal factor in the pathogenesis of cardiovascular, metabolic, and other related diseases. The regulation of endothelial dysfunction is influenced by various risk factors and intricate signaling pathways, which vary depending on the specific disease context. Despite numerous research efforts aimed at elucidating the mechanisms underlying endothelial dysfunction, the precise molecular pathways involved remain incompletely understood. This review elucidates recent research findings on the pathophysiological mechanisms involved in endothelial dysfunction, including nitric oxide availability, oxidative stress, and inflammation‐mediated pathways. We also discuss the impact of endothelial dysfunction on various pathological conditions, including atherosclerosis, heart failure, diabetes, hypertension, chronic kidney disease, and neurodegenerative diseases. Furthermore, we summarize the traditional and novel potential biomarkers of endothelial dysfunction as well as pharmacological and nonpharmacological therapeutic strategies for endothelial protection and treatment for CVD and related complications. Consequently, this review is to improve understanding of emerging biomarkers and therapeutic approaches aimed at reducing the risk of developing CVD and associated complications, as well as mitigating endothelial dysfunction.

show abstract

NR3C2 mediates oxidised low-density lipoprotein-induced human coronary endothelial cells dysfunction via modulation of NLRP3 inflammasome activation

Cited by 9 publications

References 30 publications

Inflammatory Mediators of Endothelial Dysfunction

Inflammatory Mediators of Endothelial Dysfunction

Validation of prognostic signature and exploring the immune-related mechanisms for NR3C2 in clear cell renal cell carcinoma

Endothelial dysfunction: molecular mechanisms and clinical implications

Contact Info

Product

Resources

About