Recent Highlights of
 ATVB

Dron, Jacqueline S.; Lazarte, Julieta; Hegele, Robert A.

doi:10.1161/atvbaha.118.311581

Cited by 3 publications

(2 citation statements)

References 215 publications

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“…59 The mechanism of atherosclerosis is associated with the destruction of lipoprotein metabolism and inflammation and has become the main focus of atherosclerosis research. 60 Previous studies have found that in atherosclerosis, tan-IIA acts by inhibiting low density lipoprotein (LDL) oxidation, 61 migration and development of smooth muscle cells, monocytes adhesion to the arterial endothelium, expression of proinflammatory cytokines, aggregation of platelets 62 and cholesterol accumulation mediated by macrophages. 63 However, current treatments for the inflammatory properties of atherosclerosis are still very limited.…”

Section: Pharmacological Effects Of Tanshinone-iia In Diseases Atherosclerosismentioning

confidence: 99%

Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases

Guo

et al. 2020

DDDT

169

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Salvia miltiorrhiza : (Danshen) is a significant (traditional Chinese medication) natural remedy, enhancing blood circulation and clear blood stasis. In this view, it is widely used against several heart diseases, eg, cardiomyopathy, arrhythmia, and congenital heart defects. Tanshinone IIA (tan-IIA) is the main fat-soluble component of Salvia miltiorrhiza . Modern pharmacological study shows that tan-IIA has anti-inflammatory and anti-oxidant activities. Tan-IIA induces remarkable cardioprotective effects via enhancing angiogenesis which may serve as an effective treatment against cardiovascular diseases (CVD). There is also evidence that tan-IIA has extensive immunomodulatory effects and plays a significant role in the development and function of immune cells. Tan-IIA reduces the production of inflammatory mediators and restores abnormal signaling pathways via regulating the function and activation of immune cells. It can also regulate signal transduction pathways, ie, TLR/NF-κB pathway and MAPKs/NF-κB pathway, thereby tan-IIA has an anti-inflammatory, anticoagulant, antithrombotic and neuroprotective role. It plays a protective role in the pathogenesis of cardiovascular disorders (ie, atherosclerosis, hypertension) and Alzheimer’s disease. It has also been revealed that tan-IIA has an anti-tumor role by killing various tumor cells, inducing differentiation and apoptosis, and has potential activity against carcinoma progression. In the review of this fact, the tan-IIA role in different diseases and its mechanism have been summarized while its clinical applications are also explored to provide a new perspective of Salvia miltiorrhiza . An extensive study on the mechanism of action of tan-IIA is of great significance for the effective use of Chinese herbal medicine and the promotion of its status and influence on the world.

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Section: Pharmacological Effects Of Tanshinone-iia In Diseases Atherosclerosismentioning

confidence: 99%

Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases

Guo

et al. 2020

DDDT

169

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“…The concept that atherosclerosis is a lipid-driven inflammatory disease has been supported by diverse evidence from basic and clinical research. 131,[158][159][160][161][162][163] Cell types that are involved in atherosclerosis development include leukocytes and resident cell types such as endothelial cells, smooth muscle cells, and cells in the adventitia. Although it is hard to conclude which cell type is more important than the other cell types, or one specific molecule is more important than the other multiple molecules in a single cell type, the recent studies have provided more elaborate insights into many components in the development of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Updates on Approaches for Studying Atherosclerosis

Daugherty

Lü

2019

ATVB

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Recently Developed Mouse Models-Proprotein convertase subtilisin/kexin type 9 (PCSK9) regulates LDL receptor activity. 30,69 A D374Y gain-of-function mutation in human leads to hypercholesterolemia. 70 Benefitting from the recently advances of using adeno-associated viral vectors (AAV), infection of AAVs carrying this human mutation or its mouse equivalent mutation D377Y in C57BL/6 mice has been used by many researchers to study atherosclerosis. [71][72][73][74][75][76][77][78][79][80][81] Since sex difference is an important influence on development of atherosclerosis, 82,83 some researchers have also studied potential sex difference of this method in inducing hypercholesterolemia and their contributions to atherosclerosis. 80,84 Jarrett and colleagues compared an AAV containing human PCSK9 D374Y mutation (PCSK9D374Y.AAV) to AAV vectors expressing Staphylococcus aureus Cas9 and a guide RNA targeting the Ldlr gene (AAV-CRISPR) in both male and female C57BL/6 mice. 80 Their study found that the AAV-CRISPR approach to target LDL receptors led to more profound hypercholesterolemia and increases of atherosclerosis than infection with PCSK9 D374Y.AAV in male mice, whereas PCSK9 D374Y.AAV method had more significant effects on plasma cholesterol concentrations and atherosclerosis than the AAV-CRISPR approach for LDL receptor deletion in female mice. 80 The mechanism for sex dimorphism between these two methods is unclear.Diet-related Effects-For the mouse models described above, it is common to feed these mice a diet that represents the dietary habits in Western countries. 3,[85][86][87][88] The currently available Apoe −/− mice have modest hypercholesterolemia that develop minimal atherosclerosis spontaneously. However, feeding a Western diet profoundly increases plasma cholesterol concentrations and accelerates atherosclerosis. Some laboratories also use a similar fat-enriched diet supplemented with cholesterol (1.25% wt/wt) and cholate, as discussed in the recent AHA statement. 3 Some recent studies have provided evidence that gut microbiota influence the development of atherosclerosis, [89][90][91] although findings from one study do not support that microbiota and choline-supplemented diet affect atherosclerotic lesion size in a hypercholesterolemic mouse model. 9 Irrespectively, it is important to provide detailed information including mouse housing conditions and whether diets are supplemented with choline when report atherosclerosis studies in animal models. 9,92Large Animal Models-Despite the much higher expense and difficulty in genetic manipulations, large animal models have potential benefits over mice in providing more relevant pathological and mechanistic insights into the disease in human. Three recent articles in ATVB have reported manipulations of lipoprotein metabolism and the consequences on atherosclerosis in rabbits. [93][94][95] In one study, an apoA-I-expressing helperdependent adenoviral vector delivered to carotid arteries led to reduced atherosclerosis in fat diet-fed rabbits. 93 In another st...

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Improved HDL Cholesterol through Vitamin D Status Correction Substantially Lowers 10-Year Atherosclerotic Cardiovascular Disease Risk Score in Vitamin D-Deficient Arab Adults

et al. 2023

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This interventional study aimed to determine whether correcting vitamin D status in deficient Arab adults [25(OH)D <50 nmol/L] improves their 10-year risk of Atherosclerotic Cardiovascular Disease (ASCVD) risk scores. Saudi adults (58 males 62 females) with baseline vitamin D deficiency (<50 nmol/L) were given 50,000 IU cholecalciferol weekly for 2 months, then twice a month, followed by daily 1000 IU until month 6. Fasting blood samples were collected pre- and post-intervention and assessed for glucose, lipids, and 25(OH)D levels. The predicted 10-year ASCVD risk scores were calculated at baseline and after intervention. At baseline, significantly higher 10-year ASCDV risk scores were observed in males than females (9% vs. 3%, p < 0.001). After 6 months, only 21% (25 out of 120) achieved 25(OH)D levels above optimal level (≥75 nmol/L). While modest improvements were seen in glucose and lipid profiles, only HDL cholesterol showed favorable significant changes in all participants, which translated to significantly improved 10-year ASCVD risk scores independent of whether they achieved optimum vitamin D status. Still, those who achieved optimal vitamin D levels had a modestly larger decrease in ASCVD risk scores than those with less optimal 25(OH)D levels (−23% versus −18%) and this improvement was slightly more pronounced in males (−26% versus −10%, or 16% improvement) than females (−47% versus −32%, or 15% improvement). In conclusion, vitamin D status correction significantly enhances HDL cholesterol which prospectively reduces 10-year ASCVD risk as vitamin D levels approach optimum status among adult Arabs with baseline vitamin D deficiency. This improvement appears to be slightly more apparent in males than females.

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Recent Highlights of ATVB

Cited by 3 publications

References 215 publications

<p>Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases</p>

<p>Pharmacological Activity and Mechanism of Tanshinone IIA in Related Diseases</p>

Updates on Approaches for Studying Atherosclerosis

Improved HDL Cholesterol through Vitamin D Status Correction Substantially Lowers 10-Year Atherosclerotic Cardiovascular Disease Risk Score in Vitamin D-Deficient Arab Adults

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