Statins Combined with AAV8-TBG-LOX-1 Reduce the Vascular Lipid-driven Inflammatory Response and Inhibit Atherosclerosis.

Objective: Imbalances in liver lipid metabolism and inflammatory reactions driven by oxidized lipid deposition in blood vessels constitute the core of atherosclerosis. Insufficient degradation of cholesterol in the liver promotes oxidative modification of lipid particles and their deposition on the blood vessel wall in the peripheral circulation. The blood vessel wall engulfs and processes oxidized low-density lipoprotein (Ox-LDL) as foreign matter through pattern recognition receptors, ultimately forming lipid-encapsulated plaques.

Research Progress on the Pathogenesis and Treatment of Neoatherosclerosis.

Neoatherosclerosis (NA) within stents has become an important clinical problem after coronary artery stent implantation. In-stent restenosis and in-stent thrombosis are the two major complications following coronary stent placement and seriously affect patient prognosis. As the common pathological basis of these two complications, NA plaques, unlike native atherosclerotic plaques, often grow around residual oxidized lipids and stent struts.

No evidence of coronary plaque stabilization by allopurinol in patients with acute coronary syndrome.

Background: Allopurinol, a xanthine inhibitor that lowers uric acid concentration, has been proven to reduce inflammation and oxidative stress in patients with cardiovascular disease. However, it is unknown whether these beneficial effects translate into favorable plaque modification in acute coronary syndromes (ACS). This study aimed to investigate whether allopurinol could improve coronary plaque stabilization using coronary computed tomography angiography (CCTA).

MicroRNA-146a Promotes Embryonic Stem Cell Differentiation towards Vascular Smooth Muscle Cells through Regulation of Kruppel-like Factor 4.

Objective: Vascular smooth muscle cell (VSMC) differentiation from stem cells is one source of the increasing number of VSMCs that are involved in vascular remodeling-related diseases such as hypertension, atherosclerosis, and restenosis. MicroRNA-146a (miR-146a) has been proven to be involved in cell proliferation, migration, and tumor metabolism. However, little is known about the functional role of miR-146a in VSMC differentiation from embryonic stem cells (ESCs).

Distinct Features of Gut Microbiota in High-Altitude Tibetan and Middle-Altitude Han Hypertensive Patients.

Indigenous animals show unique gut microbiota (GM) in the Tibetan plateau. However, it is unknown whether the hypertensive indigenous people in plateau also have the distinct gut bacteria, different from those living in plains. We sequenced the V3-V4 region of the gut bacteria 16S ribosomal RNA (rRNA) gene of feces samples among hypertensive patients (HPs) and healthy individuals (HIs) from 3 distinct altitudes: Tibetans from high altitude (3600-4500 m,  = 38 and 34), Hans from middle altitude (2260 m,  = 49 and 35), and Hans from low altitude (13 m,  = 34 and 35) and then analyzed the GM composition among hypertensive and healthy subgroups using the bioinformatics analysis, respectively.

Effect of active immunization against angiotensin II type 1 (AT1) receptor on hypertension & arterial remodelling in spontaneously hypertensive rats (SHR).

Background & Objectives: a0 ngiotensin II receptor type 1 (AT1) is known to be involved in the pathogenesis of hypertension. t0 his study was undertaken to explore the effect of active immunization against AT1 receptor on blood pressure and small artery remodelling in spontaneously hypertensive rat (SHR).

Methods: Male SHR and Wistar rats aged two months were actively immunized with different peptides (ATR12185ͱͲATR10014 and ATR12181) corresponding to particular sequences of rat AT1 receptor, while another SHR group was given losartan (10 mg/kg/day) orally once a day.

Enhancement of autophagy by simvastatin through inhibition of Rac1-mTOR signaling pathway in coronary arterial myocytes.

Background/aims: In addition to their action of lowering blood cholesterol levels, statins modulate biological characteristics and functions of arterial myocytes such as viability, proliferation, apoptosis, survival and contraction. The present study tested whether simvastatin, as a prototype statin, enhances autophagy in coronary arterial myocytes (CAMs) to thereby exert their beneficial effects in atherosclerosis.

Methods And Results: Using flow cytometry, we demonstrated that simvastatin significantly increased the autophagsome formation in CAMs.

Attenuation by statins of membrane raft-redox signaling in coronary arterial endothelium.

Membrane raft (MR)-redox signaling platforms associated with NADPH oxidase are involved in coronary endothelial dysfunction. Here, we studied whether statins interfere with the formation of MR-redox signaling platforms to protect the coronary arterial endothelium from oxidized low-density lipoprotein (OxLDL)-induced injury and from acute hypercholesterolemia. In cultured human coronary arterial endothelial cells, confocal microscopy detected the formation of an MRs clustering when they were exposed to OxLDL, and such MR platform formation was inhibited markedly by statins, including pravastatin and simvastatin.

Agonistic AT(1) receptor autoantibody increases in serum of patients with refractory hypertension and improves Ca(2+) mobilization in cultured rat vascular smooth muscle cells.

Agonistic AT(1) receptor autoantibodies (AT(1)-AAs) have been described in the patients with malignant hypertension or preeclampia. Furthermore, AT(1)-AAs were highly associated with refractory hypertension. Function of vascular smooth muscle cells (VSMCs) is important in the regulation of blood pressure.

The mechanism of signal transduction during vascular smooth muscle cell proliferation induced by autoantibodies against angiotensin AT1 receptor from hypertension.

Background: Autoantibodies against angiotensin AT1 receptor have been discovered in patients with preeclampsia or malignant hypertension. Some studies have demonstrated that the autoantibodies are involved in the immunopathogenesis of hypertension and have an agonist effect similar to angiotensin II.

Methods: Autoantibodies against AT1 receptor were purified from sera of patients with primary hypertension by affinity chromatography.

[Autoantibodies against alpha1 adrenergic receptor related with cardiac remodeling in hypertensive patients by clinical observation].

Objective: To investigate the effects of autoantibodies against alpha(-) adrenergic receptor on cardiac remodeling in patients with hypertension.

Methods: Five hundred and fifty three patients with hypertension in our hospital were selected. The autoantibodies against alpha(1) adrenergic receptor in sera of donor were detected by ELISA, and the results of echocardiography were recorded.

Target organ protection from a novel angiotensin II receptor (AT1) vaccine ATR12181 in spontaneously hypertensive rats.

Hypertension produces pathophysiological changes that are often responsible for the mortality associated with the disease. It is evident that overactive renin-angiotensin systems play a central role in the development of hypertension and target organ damage associated with hypertension. We have previously found that a novel angiotensin II receptor (AT1) vaccine-ATR12181 attenuated the development of high blood pressure (BP) in spontaneously hypertensive rat (SHR) model of human essential hypertension.

Autoantibodies against AT1-receptor and alpha1-adrenergic receptor in patients with hypertension.

This study will explore the autoantibodies against AT1-receptor and alpha1-adrenergic receptor in patients with hypertension. Forty normotensives and 194 patients with hypertension were recruited for participation in this study. All patients accepted systemic combination drug treatment for antihypertension.