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.

[Association of Cystatin C and metabolic syndrome].

Objective: To explore the correlation between serum levels of Cystatin C and metabolic syndrome.

Methods: This study was randomly conducted in 506 persons, including 191 patients with metabolic syndrome (MS), 210 with metabolic disorder (MD) and 105 persons in normal control (NC) group. According to serum levels of Cys C, the clinical data were also divided into 3 groups of lower tertile (T1, n = 165), middle tertile (T2, n = 172) and upper tertile (T3, n = 169).

The role of TWEAK/Fn14 in cardiac remodeling.

The pathophysiological basis of heart failure is cardiac remodeling, a process that comprises structural and functional changes including cardiomyocyte proliferation, hypertrophy, necrosis, apoptosis, autophagy, interstitial fibrosis, contractile dysfunction and ventricular dilatation. Accumulating evidence demonstrate that tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is involved in the process by binding its receptor fibroblast growth factor-inducible molecule 14 (Fn14). In this review, we will discuss the potential role of the TWEAK/Fn14 axis in cardiac remodeling, elucidate its possible mechanisms and explore new therapeutic targets for heart failure.

TWEAK/Fn14 promotes the proliferation and collagen synthesis of rat cardiac fibroblasts via the NF-кB pathway.

We wished to elucidate a potential role of the tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible molecule 14 (Fn14) axis in myocardial fibrosis. Stimulation of neonatal rat cardiac fibroblasts (CFs) with TWEAK could increase CFs numbers and collagen synthesis. Conversely, when CFs were pretreated with siRNA against Fn14, induction of cell proliferation and collagen synthesis by TWEAK were inhibited.

[The correlation of human serum Lp-PLA2 and hs-CRP and stability of coronary atherosclerotic plaques].

Objective: To explore the relationship of serum lipoprotein-associated phospholipase A2 and high sensitive C-reactive protein in vulnerable coronary atherosclerotic plaques.

Methods: Patients undergoing coronary angiography (CAG) were examined for CAD with intravascular ultrasound (IVUS). According to the findings of CAG and IVUS, all the patients were divided into three groups: a control group without plaque, stable plaque group and vulnerable plaque group.

Increased plasma osteoprotegerin levels are associated with the presence and severity of acute coronary syndrome.

Objective: The objective of this study was to explore the relationship between increased plasma osteoprotegerin (OPG) levels and acute coronary syndrome (ACS).

Methods: Plasma OPG levels from 85 subjects undergoing coronary artery angiography in three different groups, including ACS (n=45), stable angia pectoris (SAP) (n=20) and normal coronary artery (NCA) (n=20), were detected by ELISA. Twenty-two ascending aorta specimens were surgically taken from 8 ACS, 7 SAP and 7 NCA patients, and OPG mRNA expression in the specimens was detected by RT-PCR.

A high association of aortic valve sclerosis detected by transthoracic echocardiography with coronary arteriosclerosis.

Objective: To examine whether aortic valve sclerosis (AVS) detected by transthoracic echocardiography (TTE) has a high association with coronary arteriosclerosis.

Methods: Clinical and angiographic features and TTE findings were retrospectively analyzed in a blinded fashion for 138 consecutive patients, of whom 58 had AVS and 80 had non-AVS diseases. Both histological and immunohistochemical studies were performed on frozen aortic valve sections obtained at autopsy from 7 AVS and 3 non-AVS patients.