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In contrast, the lowest risk of cardiovascular mortality and MI was observed at the extreme high end. In men, there was a significant inverse and graded increase in hazard ratios of all outcomes in the lower HDL-C categories compared to the reference group (50-59 mg/dL). In the higher HDL-C categories, no significant increase in outcomes was observed. Women showed similar trends.

The risk of mortality, MI, and stroke was high at low HDL-C levels in the Korean general population. However, extremely high HDL-C levels were not associated with an increased risk of mortality, MI, and stroke.

The risk of mortality, MI, and stroke was high at low HDL-C levels in the Korean general population. However, extremely high HDL-C levels were not associated with an increased risk of mortality, MI, and stroke.

Vascular calcification requires the differentiation of vascular smooth muscle cells (VSMCs) into osteoblast-like cells. This phenomenon can be enhanced by inflammation and oxidative stress. Zingerone is one of the active ingredients present in the ginger plant that has anti-inflammatory and antioxidant effects. Other functions include anti-obesity, anti-nausea effects. However, the functions of zingerone on vascular calcification has not yet been elucidated. This study investigated the effect of zingerone on vascular calcification and its molecular mechanism.

Reverse transcription-polymerase chain reaction (PCR), real-time PCR and Western blot analysis was used to measure expression levels of osteogenic marker genes and to investigate whether calcification was regulated by the expression of AMP-activated protein kinase (AMPK) and tissue inhibitor of metalloproteinase 4 (TIMP4). Alizarin red S staining was used to measure calcium deposition. Studies were carried out in VSMCs.

Zingerone induced the expresnaling cascade in VSMCs. These results suggest that the natural product zingerone could be useful for treating vascular and metabolic diseases.Dyslipidemia related diseases such as hyperlipidemia and atherosclerosis are the leading cause of death in humans. While cellular and molecular basis on the pathophysiology of dyslipidemia has been extensively investigated over decades, we still lack comprehensive understanding on the etiology of dyslipidemia due to the complexity and the innate multimodality of the diseases. While mouse has been the model organism of choice to investigate the pathophysiology of human dyslipidemia, zebrafish, a small freshwater fish which has traditionally used to study vertebrate development, has recently emerged as an alternative model organism. In this review, we will provide comprehensive perspective on zebrafish as a model organism for human dyslipidemia; we will discuss the attributes of zebrafish as a model, and compare the lipid metabolism in zebrafish and humans. In addition, we will summarize current landscape of zebrafish-based dyslipidemia research.A single layer of squamous endothelial cells (ECs), the endothelium, regulates the flow of substance and fluid into and out of a tissue. Toyocamycin mouse The endothelium is also involved in vasculogenesis, the formation of new blood vessels, which is a crucial process for organ development in the embryo and fetus. Because most murine mutations of genes involved in EC development cause early embryo lethality, EC-specific conditional knockout (cKO) mouse models are indispensable for in vivo studies. cKO mice including the floxed allele can be generated through advanced approaches including embryonic stem cell-mediated gene targeting or the CRISPR/Cas system. EC-specific mouse models can be generated through further breeding of floxed mice with a Cre driver line, the latest information of which is available in the Jackson Cre Repository or the EUCOMMTOOLS project. Because it takes a long time (generally 1-2 years) to generate EC-specific mouse models, researchers must thoroughly design and plan a breeding strategy before full-scale mouse experiments, which saves time and money for in vivo study. In summary, revolutionary technical advances in embryo manipulation and assisted reproduction technologies have made it easier to generate EC-specific mouse models, which have been used as essential resources for in vivo studies of the endothelium.This review focuses on the role of adipose tissue in obese individuals in the development of metabolic diseases, and their consequences for metabolic and functional derangements in the heart. The general idea is that the expansion of adipocytes during the development of obesity gives rise to unhealthy adipose tissue, characterized by low-grade inflammation and the release of proinflammatory adipokines and fatty acids (FAs). This condition, in turn, causes systemic inflammation and elevated FA concentrations in the circulation, which links obesity to several pathologies, including impaired insulin signaling in cardiac muscle and a subsequent shift in myocardial substrate oxidation in favor of FAs and reduced cardiac efficiency. This review also argues that efforts to prevent obesity-related cardiometabolic disease should focus on anti-obesogenic strategies to restore normal adipose tissue metabolism.Mitochondrial fatty acid β-oxidation (mFAO), which is the major pathway for the degradation of fatty acids and is critical for maintaining energy homeostasis in the human body, consists of carnitine transport, the carnitine shuttle, and fatty acid β-oxidation. Inherited metabolic defects of mFAO result in more than 15 distinct mFAO disorders (mFAODs) with varying clinical manifestations. The common elements of the clinical presentation of mFAODs are hypoketotic hypoglycemia, (cardio)myopathy, arrhythmia, and rhabdomyolysis, indicating the importance of FAO during fasting or stressful situations. The management of all mFAODs includes avoidance of fasting, aggressive treatment during illness, and supplementation of carnitine or appropriate nutritional support, if necessary. Through the introduction of newborn screening using tandem mass spectrometry, early identification of mFAODs became feasible, leading to an early initiation of treatment with improved outcomes. However, many unmet needs remain with regard to the long-term management of patients with mFAODs.