[Effects of inhibition of Rho/ROCK pathway on proliferation and migration of airway smooth muscle cells and related mechanisms].

Objectives: To investigate the effects and molecular mechanisms of inhibition of the Ras homolog gene (Rho)/Rho-associated coiled-coil forming protein kinase (ROCK) pathway on the proliferation and migration of airway smooth muscle cells involving myocardin (MYOCD).

Methods: Human airway smooth muscle cells were infected with the adenoviral vector Ad-ZsGreen-shRNA-hROCK1 . The cells were randomly divided into four groups: gene silencing control (shNC) group, shNC + arachidonic acid (AA, Rho/ROCK pathway activator) group, gene silencing (shROCK1) group, and shROCK1 + AA group (=3 each).

Structural evolution and electronic properties of neutral and anionic TiASi (A = Sc, Ti; ≤ 12): relatively stable TiASi as a structural unit.

Simulated photoelectron spectroscopy was conducted to investigate the structural evolution and electronic properties of TiASi (A = Sc, Ti; ≤ 12) clusters and their anions the Perdew-Burke-Enzerhof scheme and extensive cluster search using the ABCluster software. The results revealed that the ground-state structures of the TiASi (A = Sc, Ti) clusters generally exhibited similar configurations except for the TiSi, ScTiSi, and TiScSi clusters. Furthermore, the TiASi clusters exhibited an adsorptive evolution pattern, and the TiASi unit was considered the basic constituent framework of the structure, excluding several distortions and minor changes.

Diagnosis, treatment, and prevention of monkeypox in children: an experts' consensus statement.

Monkeypox is a zoonotic disease. Since the first human monkeypox case was detected in 1970, it has been prevalent in some countries in central and western Africa. Since May 2022, monkeypox cases have been reported in more than 96 non-endemic countries and regions worldwide.

Quantum chemistry calculations of the growth patterns, simulated photoelectron spectra, and electronic properties of LaASi (A = Sc, Y, La; ≤ 10) compounds and their anions.

The growth patterns, simulated photoelectron spectra, and electronic properties of LaASi (A = Sc, Y, and La; ≤ 10) compounds and their anions were studied quantum chemistry calculations using the Perdew-Burke-Ernzerhof (PBE) method and unprejudiced structural searching software ABCluster. The results revealed that the growth patterns of the most stable structures of neutral and anionic LaASi showed an adsorptive mode. The lowest-energy structures (LESs) of the LaASi ( ≤ 7) clusters were similar, except for those of anionic LaYSi and LaYSi and neutral LaScSi.

[Effects of GPR81 agonist on insulin resistance in rats with nonalcoholic fatty liver disease].

To investigate the effects of NOD-like receptor protein 3 (NLRP3) signaling pathway on insulin resistance and the intervention of lactic acid receptor G protein-coupled receptor 81 (GPR81) agonist in nonalcoholic fatty liver disease (NAFLD) rats. Thirty SD male rats were randomly divided into three groups: control group, NAFLD group and GPR81 agonist group, with 10 rats in each group. Nonalcoholic fatty liver rat model was established by high fat diet.

Protein deglycase DJ-1 deficiency induces phenotypic switching in vascular smooth muscle cells and exacerbates atherosclerotic plaque instability.

Protein deglycase DJ-1 (DJ-1) is a multifunctional protein involved in various biological processes. However, it is unclear whether DJ-1 influences atherosclerosis development and plaque stability. Accordingly, we evaluated the influence of DJ-1 deletion on the progression of atherosclerosis and elucidate the underlying mechanisms.

Inhibition of Rho-kinase is involved in the therapeutic effects of atorvastatin in heart ischemia/reperfusion.

The aim of the present study was to investigate the effects of atorvastatin against heart ischemia/reperfusion (I/R) injury and its potential underlying mechanism. Rats were allocated into the following groups: Sham, I/R, atorvastatin (10 mg/kg daily), fasudil (10 mg/kg daily) and atorvastatin + fasudil in combination. Drugs were administered for 2 weeks prior to I/R injury.

Correction: Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Loss of PARP-1 attenuates diabetic arteriosclerotic calcification via Stat1/Runx2 axis.

Accelerated atherosclerotic calcification is responsible for plaque burden, especially in diabetes. The regulatory mechanism for atherosclerotic calcification in diabetes is poorly characterized. Here we show that deletion of PARP-1, a main enzyme in diverse metabolic complications, attenuates diabetic atherosclerotic calcification and decreases vessel stiffening in mice through Runx2 suppression.

Serum cystatin C levels relate to no-reflow phenomenon in percutaneous coronary interventions in ST-segment elevation myocardial infarction.

Background/aim: No-reflow is a serious and frequent event during primary percutaneous coronary intervention (PPCI) for acute ST segment elevation myocardial infarction (STEMI). The aim of this study was to identify possible predictors for no-reflow.

Patients And Methods: We investigated 218 patients with acute anterior STEMI who underwent PPCI from December 2016 to December 2018.

Predictive value of fasting blood glucose for serious coronary atherosclerosis in non-diabetic patients.

Objective: To determine if high fasting blood glucose (FBG) level is an independent predictor of serious coronary lesions in patients with coronary artery disease (CAD).

Methods: We enrolled 64 patients who had symptoms of chest discomfort and who underwent coronary angiography. FBG was determined from blood samples and the extent of coronary artery lesions was analyzed according to Gensini score.

Increased Rho kinase activity in patients with heart ischemia/reperfusion.

Background/aim:\: Rho kinase is a downstream effector of Rho GTPase that is known to regulate various pathological processes. The aim of this study was to evaluate the regulation of Rho kinase activity in leukocytes in patients with ischemia/reperfusion (I/R) injury.

Patients And Methods: We investigated 38 patients with acute ST-segment elevation myocardial infarction (STEMI), 26 patients with atherosclerosis (AS) and 22 normal subjects.

Irisin inhibits high glucose-induced endothelial-to-mesenchymal transition and exerts a dose-dependent bidirectional effect on diabetic cardiomyopathy.

Emerging evidence indicates that irisin provides beneficial effects in diabetes. However, whether irisin influences the development of diabetic cardiomyopathy (DCM) remains unclear. Therefore, we investigated the potential role and mechanism of action of irisin in diabetes-induced myocardial dysfunction in mice.

Ulinastatin attenuates diabetes-induced cardiac dysfunction by the inhibition of inflammation and apoptosis.

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms.

Novel 6-bp deletion in MEF2A linked to premature coronary artery disease in a large Chinese family.

The aim of the present study was to identify the genetic defect responsible for familial coronary artery disease/myocardial infarction (CAD/MI), which exhibited an autosomal dominant pattern of inheritance, in an extended Chinese Han pedigree containing 34 members. Using exome and Sanger sequencing, a novel 6‑base pair (bp) 'CAGCCG' deletion in exon 11 of the myocyte enhancer factor 2A (MEF2A) gene was identified, which cosegregated with CAD/MI cases in this family. This 6‑bp deletion was not detected in 311 sporadic cases of premature CAD/MI or in 323 unrelated healthy controls.

Inhibition of myocyte-specific enhancer factor 2A improved diabetic cardiac fibrosis partially by regulating endothelial-to-mesenchymal transition.

Cardiac fibrosis is an important pathological process of diabetic cardiomyopathy, the underlying mechanism remains elusive. This study sought to identify whether inhibition of Myocyte enhancer factor 2A (MEF2A) alleviates cardiac fibrosis by partially regulating Endothelial-to-mesenchymal transition (EndMT). We induced type 1 diabetes mellitus using the toxin streptozotocin (STZ) in mice and injected with lentivirus-mediated short-hairpin RNA (shRNA) in myocardium to inhibit MEF2A expression.

Darapladib, a Lipoprotein-Associated Phospholipase A2 Inhibitor, Reduces Rho Kinase Activity in Atherosclerosis.

Purpose: Increased lipoprotein-associated phospholipase A2 (Lp-PLA2) activity and Rho kinase activity may be associated with atherosclerosis. The principal aim of this study was to examine whether darapladib (a selective Lp-PLA2 inhibitor) could reduce the elevated Lp-PLA2 and Rho kinase activity in atherosclerosis.

Materials And Methods: Studies were performed in male Sprague-Dawley rats.

Prohibitin overexpression improves myocardial function in diabetic cardiomyopathy.

Prohibitin (PHB) is a highly conserved protein implicated in various cellular functions including proliferation, apoptosis, tumor suppression, transcription, and mitochondrial protein folding. However, its function in diabetic cardiomyopathy (DCM) is still unclear. In vivo, type 2 diabetic rat model was induced by using a high-fat diet and low-dose streptozotocin.

Poly(ADP-ribose)polymerase 1 inhibition protects against age-dependent endothelial dysfunction.

Age-related endothelial dysfunction is closely associated with the local production of reactive oxygen species (ROS) within and in the vicinity of the vascular endothelium. Oxidant-induced DNA damage can activate the nuclear enzyme poly(ADP-ribose) polymerase 1 (PARP-1), leading to endothelial dysfunction in various pathophysiological conditions. The present study aimed to investigate the role of PARP-1 in age-dependent changes in endothelial cell function and its underlying mechanism.

Therapeutic effects of the soluble epoxide hydrolase (sEH) inhibitor AUDA on atherosclerotic diseases.

In this study, we aimed to detect the effects of the soluble epoxide hydrolase (sEH) inhibitor 12-(3-adamantan-1-yl-ureido)-dodecanoic acid (AUDA) on atherosclerotic diseases and to explore its mechanism. The atherosclerosis animal model was constructed by ApoE-/- mice. To determine the optimal therapeutic concentration of AUDA, different concentrations of AUDA were infused into ApoE-/- mice, with controls receiving infusions of normal saline alone.

Atorvastatin counteracts high glucose-induced Krüppel-like factor 2 suppression in human umbilical vein endothelial cells.

Objective: Krüppel-like factor 2 (KLF2) is a transcription factor that regulates endothelial function and atorvastatin can stabilize atherosclerotic plaque and inhibit inflammation on endothelial cells by attenuating the role of cytokines. The aim of this study is to investigate the effect of high glucose (HG) on KLF2 expression in human umbilical vein endothelial cells (HUVECs) and the underlying mechanisms.

Methods: HUVECs were isolated from the human umbilical cords from normal pregnancies and exposed to medium containing 25.

The application of vWF/ADAMTS13 in essential hypertension.

Background: Plasma von Willebrand factor (vWF), a key player in hemostasis and thrombosis, is released from endothelial cells during inflammation. Hypertension, a progressing in chronic inflammation and cardiovascular syndrome with various causes, results in functional and structural changes of heart and arterial vessels. However little information is available on LA changes during hypertension.

Rho-kinase inhibition is involved in the activation of PI3-kinase/Akt during ischemic-preconditioning-induced cardiomyocyte apoptosis.

Unlabelled: We and others have reported that Rho-kinase plays an important role in the pathogenesis of heart ischemia/reperfusion (I/R) injury. Studies also have demonstrated that the activation of Rho-kinase was reversed in ischemic preconditioning (IPC). This study aimed to explain the mechanism of Rho-kinase-mediated cardiomyocyte apoptosis increased in I/R and reversed in IPC.