Irisin in atherosclerosis.

Irisin, a novel exercise-induced myokine, has been shown to play important roles in increasing white adipose tissue browning, regulating energy metabolism and improving insulin resistance. Growing evidence suggests a direct role for irisin in preventing atherosclerosis (AS) by inhibiting oxidative stress, improving dyslipidemia, facilitating anti-inflammation, reducing cellular damage and recovering endothelial function. In addition, some studies have noted that serum irisin levels play an essential role in cardiovascular diseases (CVDs) risk prediction, highlighting that irisin has the potential to be a useful predictive marker and therapeutic target of AS, especially in monitoring therapeutic efficacy. This review summarizes the understanding of irisin-mediated regulation in essential biological pathways and functions in atherosclerosis and prompts further exploitation of the biological properties of irisin in the pathogenesis of atherosclerosis.

Angiopoietin-like proteins in atherosclerosis.

Atherosclerosis, as a chronic inflammatory disease within the arterial wall, is a leading cause of morbidity and mortality worldwide due to its role in myocardial infarction, stroke and peripheral artery disease. Additional evidence is emerging that the angiopoietin-like (ANGPTL) family of proteins participate in the pathology of this disease process via endothelial dysfunction, inflammation, dyslipidemia, calcification, foam cell formation and platelet activation. This review summarizes current knowledge on the ANGPTL family of proteins in atherosclerosis related pathological processes. Moreover, the potential value of ANGPTL family proteins as predictive biomarkers in atherosclerosis is discussed. Given the attractive role of ANGPTL3, ANGPTL4, ANGPTL8 in atherosclerotic dyslipidemia via regulation of lipoprotein lipase (LPL), antisense oligonucleotide or/and monoclonal antibody-based inactivation of these proteins represent potential atherosclerotic therapies.

Chemerin in atherosclerosis.

Atherosclerosis (AS), a chronic arterial disease, is characterized by endothelial dysfunction, inflammatory reactions and lipid accumulation in parallel with aberrant angiogenesis and vascular smooth muscle cell (VSMC) proliferation. Adipose tissue has been suggested to have an integral influence on metabolism and endocrine secretion, while there have been increasing concerns about the possible involvement of adipokines in cardiovascular diseases, including AS. Here, we focused on chemerin, an adipokine highly expressed in adipose tissue, with strong evidence of an association with inflammation, endothelial dysfunction, metabolic disorder, aberrant angiogenesis, VSMC proliferation and calcification. In this review, we discuss chemerin and its receptors in the pathogenesis of AS. However, the existing data assign various, even contradictory, roles to chemerin in atherosclerosis, such as inhibiting vascular calcification and impairing endothelial function. Current studies focusing on its anti- and pro-atherogenic effects have pinpointed its distinct role in specific cell types and contexts in the pathogenesis of atherosclerosis. Therefore, the gaps in current knowledge regarding the specific role played by chemerin in the etiology of AS require additional future studies. It seems reasonable to suggest that targeted chemerin therapy can be developed as an innovative approach for treating AS.

Adipokines in vascular calcification.

Adipose tissue (AT), a critical endocrine gland, is capable of producing and secreting abundant adipokines. Adipokines act on distant or adjacent organ tissues via paracrine, autocrine, and endocrine mechanism, which play attractive roles in the regulation of glycolipid metabolism and inflammatory response. Increasing evidence shows that adipokines can connect obesity with cardiovascular diseases by serving as promoters or inhibitors in vascular calcification. The chronic hypoxia in AT, caused by the adipocyte hypertrophy, is able to trigger imbalanced adipokine generation, which leads to apoptosis, osteogenic differentiation of vascular smooth muscle cells (VSMCs), vascular inflammation, and abnormal deposition of calcium and phosphorus in the vessel wall. The objectives of this review aim at providing a brief summary of the crucial influence of major adipokines on the formation and development of vascular calcification, which may contribute to better understanding these adipokines for establishing the appropriate therapeutic strategies to counteract obesity-associated vascular calcification.

Image routing via atomic spin coherence.

Coherent storage of optical image in a coherently-driven medium is a promising method with possible applications in many fields. In this work, we experimentally report a controllable spatial-frequency routing of image via atomic spin coherence in a solid-state medium driven by electromagnetically induced transparency (EIT). Under the EIT-based light-storage regime, a transverse spatial image carried by the probe field is stored into atomic spin coherence. By manipulating the frequency and spatial propagation direction of the read control field, the stored image is transferred into a new spatial-frequency channel. When two read control fields are used to retrieve the stored information, the image information is converted into a superposition of two spatial-frequency modes. Through this technique, the image is manipulated coherently and all-optically in a controlled fashion.

Three new naphthalenyl glycosides from the root bark of Juglans cathayensis.

Phytochemical investigations of the root bark of Juglans cathayensis DODE. led to the isolation of three new naphthalenyl glycosides, Jugnaphthalenoside A-C (1-3). Their structures were elucidated on the basis of extensive analysis of spectroscopic data. The cytotoxicities of the three new compounds were also evaluated.

Schiglautone A, a new tricyclic triterpenoid with a unique 6/7/9-fused skeleton from the stems of Schisandra glaucescens.

Schiglautone A (1), a unique 6/7/9-fused tricyclic carbon backbone triterpenoid, was isolated from the stems of Schisandra glaucescens. Its structure was determined on the basis of spectroscopic analysis and single-crystal X-ray crystallography. A hypothetical biosynthetic pathway of 1 was postulated.