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Impact of Dietary Polyphenols on Arterial Stiffness
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Tess De Bruyne, Lynn Roth, Harry Robberecht, Luc Pieters, Guido De Meyer, Nina Hermans
Inflammation is involved in arterial stiffness development by multiple mechanisms. Low-grade inflammation impairs endothelial function by reducing NO bioavailability and increasing endothelin-1, thus contributing to progressive arterial stiffening, which, in turn, further impairs endothelial function (Avolio, 2013). The contribution of an inflammatory status is furthermore reflected in the role of MMPs in elastin degradation, the overexpression of lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) (by an NF-κB dependent mechanism), increasing uptake of oxidized low-density lipoprotein (oxLDL), the transdifferentiation of VSMCs into an osteoblastic phenotype under inflammatory conditions, influence of cytokines, increased AGEs synthesis, C-reactive protein (CRP: inhibits endothelial NO synthase, increases cytokine expression, increases generation of ROS), influence of adhesion molecules, microRNAs and so on. (Mozos et al., 2017a). Chronic low-grade inflammation interacts synergistically with oxidative stress, but the order and relationship between these events are uncertain (LaRocca et al., 2017).
Osteoarthritis
Published in Kohlstadt Ingrid, Cintron Kenneth, Metabolic Therapies in Orthopedics, Second Edition, 2018
David Musnick, Richard D. Batson
Previous research has demonstrated reduced serum HDL cholesterol levels in OA patients (Soran et al., 2008). Recent research has shown a significant inverse relationship between HDL cholesterol levels and risk of hand osteoarthritis (Garcia-Gil et al., 2017). Obesity-related dyslipidemia is also characterized by elevated oxidized LDL. Oxidized LDL has been shown to induce joint inflammation and cartilage destruction via activation of the Ox-LDL receptor-1 (LOX-1). Activation of the LOX-1 by oxidized LDL stimulates the release of vascular endothelial growth factor (VEGF), thereby increasing the expression of inflammatory cytokines IL-1β, IL-6 and TNF-α. In addition, Ox-LDL can directly induce matrix metalloproteinases (MMP), leading to further cartilage degradation, while decreasing chondrocyte cell viability and proteoglycan synthesis.
Preclinical evaluation of multimodality probes
Published in Yi-Hwa Liu, Albert J. Sinusas, Hybrid Imaging in Cardiovascular Medicine, 2017
In addition to direct labeling with radioisotopes, new radionuclide nanoparticles are being developed for targeted imaging to enable noninvasive detection, diagnosis, and monitoring disease progression. These probes will share the high sensitivity of traditional radiotracers but also have a high specificity due to surface chemistry conjugation and will likely be readily clinically translatable. In one study, de Baross et al. synthesized 125I-labeled dextran-coated iron oxide nanoparticles to detect macrophages in the atherosclerosis plaques of coronary arteries (de Barros et al. 2014). A biodistribution study showed significant accumulation of the probe in the heart of apoE−/− mice (de Barros et al. 2014). In another study, Li et al. reported the use of 111In-labeled liposome nanoparticles with surface conjugation with antibodies against the low-density lipoprotein receptor LOX1. SPECT imaging displayed a “hot spot” signal in atherosclerotic plaques in apoE−/− mice (Li et al. 2010).
Angiotensin II type 2 receptor prevents extracellular matrix accumulation in human peritoneal mesothelial cell by ameliorating lipid disorder via LOX‐1 suppression
Published in Renal Failure, 2022
Jing Liu, Bo Jin, Jian Lu, Yuan Feng, Nan Li, Cheng Wan, Qing-Yan Zhang, Chun-Ming Jiang
Our previous study demonstrated that HG stimulates intracellular Ang II/AT1 signaling to induce disruption of low-density lipoprotein receptor (LDLr) negative feedback regulation. Subsequently, this dysregulation led to lipid deposition in HPMCs, thereby promoting ECM production [12]. To our knowledge, AT2 is thought to antagonisticly affect AT1 function, AT2 has been proven to improve lipid metabolism and prevent adiposity [13]. Sourashish et al. demonstrated that pharmacological activation of AT2 prevented high-fat diet-induced adiposity, dyslipidemia and inflammation and insulin resistance. The results indicate AT2 as a potential therapeutic approach for controlling obesity and obesity-associated disorders [14]. Recent studies have shown that there is a close relationship between lectin-like oxidized low-density lipoprotein scavenger receptor-1 (LOX-1) and AT2 [15,16]. LOX-1 is one of the important receptors responsible for binding, internalizing and degrading oxidized LDL (ox-LDL) [17]. The activation of LOX-1 is known to be connected with some pathophysiological events, including endothelial injury and dysfunction, fibroblast growth, and vascular smooth muscle cell hypertrophy. Many of these pathologic changes are involved in atherosclerosis [18], hypertension [19], and myocardial ischemia and remodeling [20]. Nevertheless, whether the decrease in AT2 levels facilitates the disruption of lipid homeostasis by LOX-1 and mediates peritoneal injury has not been explored.
LOX-1 Regulates Neutrophil Apoptosis and Fungal Load in A. Fumigatus Keratitis
Published in Current Eye Research, 2021
Cui Li, Kun He, Min Yin, Qiuqiu Zhang, Jing Lin, Yawen Niu, Qian Wang, Qiang Xu, Nan Jiang, Guiqiu Zhao
Fungal keratitis (FK) is infectious corneal disease with high rate of blindness.1 When infected with pathogenic fungi, the host activates the immune system to recognize and eliminutesate these pathogenic fungi. As important pattern recognition receptors (PRRs), C-type lectin receptors play a crucial regulatory role in fungal keratitis.2–5 Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1), is one of type II membrane proteins and structurally belongs to C-typed lectin family. It includes a short intracellular N-terminus hydrophilic domain and a long extracellular C- terminus hydrophilic domain. The specific structure enables LOX-1 to recognize specific substances, including pathogenic microorganisms, oxidized low-density lipoproteins (ox-LDLs), endotoxins, damaged or apoptosis cells, suggesting that LOX-1 involves in immune response through different ways.6
ERK1/2-PPARγ pathway is involved in Chlamydia pneumonia-induced human umbilical vein endothelial cell apoptosis through increased LOX-1 expression
Published in Journal of Receptors and Signal Transduction, 2020
Shan Sun, Xiaoyu Duan, Qinqin Wu, Yingxia He, Xiaofen Bu, Xiaoyan Ming, Fengqin Yan, Hong Zhu
In the present study, we showed that C.pn-induced LOX-1 expression in HUVECs (Figure 1). This is consistent with the results of previous studies performed using C.pn-infected human endothelial cells [19]. Moreover, Campbell et al. reported that C.pn infection induce the expression of LOX-1 and pro-atherogenic factors, such as matrix metalloproteinases (MMP-1 and MMP-3), in HUVECs [20]. The role of LOX-1 in AS has been established, as the activation of the LOX-1 receptor is involved in a plethora of events that contribute to the atherosclerotic process [21]. Activation of LOX-1 in endothelial cells leads to endothelial dysfunction, cell damage, and apoptosis [22]. We also verified that C.pn infection induced apoptosis and inhibited cell proliferation in HUVECs (Figure 2(C,D)). Our findings suggested that C.pn infection resulted in HUVEC injury and apoptosis by increasing the expression of LOX-1.