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Fish oil attenuates the expression of the CCL2 chemokine and histone-modifying enzymes in LPS-stimulated human preadipocytes.
Metabol Open
December 2024
Post-graduate Program in Chemical Biology - Institute of Environmental Sciences, Chemical and Pharmaceutical, Federal University of São Paulo - UNIFESP, Diadema, Brazil.
In obesity, C-C chemokine ligand 2 (CCL2) plays a critical role in recruiting macrophages to white adipose tissue (WAT), contributing to chronic inflammation. In this study, we sought to explore the effects of fish oil (FO) on CCL2 expression and histone (H3K27)-modifying enzymes in both human model of preadipocytes and primary adipose-derived stem cells (ASCs). Present findings in preadipocytes lineage evidenced that lipopolysaccharide (LPS) increased (∼5.
View Article and Find Full Text PDFA Minimally-Invasive Swine Model of Chronic Kidney Disease-Associated Heart Failure.
Am J Physiol Heart Circ Physiol
December 2024
Cardiovascular Research Institute, Icahn School of Medicine at Mount Sinai, New York, NY.
Background: Chronic kidney disease (CKD) is on the rise, and over 50% of patients die from cardiac causes. Patients develop heart failure due to unelucidated reno-cardiac interactions, termed type 4 cardiorenal syndrome (CRS4). The aim of this study is to establish and characterize a reliable model of CRS4 in swine with marked cardiac diastolic dysfunction.
View Article and Find Full Text PDFConditional ablation of MCU exacerbated cardiac pathology in a genetic arrhythmic model of CPVT.
J Mol Cell Cardiol Plus
December 2024
Department of Biological Sciences, Mississippi State University, Starkville, MS 39762, USA.
Background: Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a genetic arrhythmic syndrome caused by mutations in the calcium (Ca) release channel ryanodine receptor (RyR2) and its accessory proteins. These mutations make the channel leaky, resulting in Ca-dependent arrhythmias. Besides arrhythmias, CPVT hearts typically lack structural cardiac remodeling, a characteristic often observed in other cardiac conditions (heart failure, prediabetes) also marked by RyR2 leak.
View Article and Find Full Text PDFPulmonary veno-occlusive disease (PVOD) is a lethal variant of pulmonary hypertension. The degree of pulmonary arterial involvement varies. Here, we compare two PVOD patients who were transplanted at 8 years of age, whereof one is a homozygous mutation carrier.
View Article and Find Full Text PDFSilencing N29 Regulated miR-193b-5p/TGFBR2 Axis to Mitigate the Progression of Cardiac Hypertrophy.
J Gene Med
December 2024
School of Medicine, Nankai University, Tianjin, China.
The study aimed to analyze differentially expressed lncRNAs in a model of cardiac hypertrophy, specially focusing on the molecular mechanisms of lncRNA NONMMUT023529 (lncRNA N29) in myocardial hypertrophy. Based on gene microarray results, RT-qPCR validation confirmed that lncRNA N29 was significantly upregulated in TAC-induced mice cardiac tissues. Echocardiographic assessments further verified that silencing lncRNA N29 led to a marked improvement in cardiac function, which aligned with the pathological findings revealed by H&E and Masson staining.
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