Background: Ribosome biogenesis (RiboSis) is a complex process for generating ribosomes, the cellular machinery responsible for protein synthesis. Dysfunctional RiboSis can disrupt cardiac structure and function, contributing to cardiovascular diseases. This study employed a Mendelian randomization (MR) approach, integrating multi-omics data, to investigate the relationship between RiboSis-related genes and standard cardiac structure and function.
View Article and Find Full Text PDFBackground And Objectives: Acute aortic syndrome (AAS) is a life-threatening condition in which there is a fracture in the integrity of the aortic wall. gamma-glutamyl transferase to lymphocyte ratio (GLR) is recognized as a risk factor for liver cirrhosis, fibrosis, and hepatocellular carcinoma. However, there are no clinical reports of GLR and AAS.
View Article and Find Full Text PDFBackground: Acute kidney injury (AKI) is a prevalent complication of acute aortic dissection (AAD) and is associated with poor outcomes. The onset of AAD may result in endothelial injury due to the formation of the false lumen, which can activate the coagulation pathway and lead to coagulation dysfunction. It serves as a valuable diagnostic and prognostic marker for AAD, but also plays a role in the pathological mechanisms underlying AKI.
View Article and Find Full Text PDFBMC Med Genomics
October 2021
Background: Both DNA genotype and methylation of antisense non-coding RNA in the INK4 locus (ANRIL) have been robustly associated with coronary artery disease (CAD), but the interdependent mechanisms of genotype and methylation remain unclear.
Methods: Eighteen tag single nucleotide polymorphisms (SNPs) of ANRIL were genotyped in a matched case-control study (cases 503 and controls 503). DNA methylation of ANRIL and the INK4/ARF locus (p14, p15 and p16) was measured using pyrosequencing in the same set of samples (cases 100 and controls 100).
Aims: Renin-angiotensin system modulates cardiac structure independent of blood pressure. The present study aimed at investigating whether single nucleotide polymorphism (SNP) and haplotype of angiotensin converting enzyme 2 (ACE2) could influence blood pressure and the susceptibility to hypertensive left ventricular hypertrophy (LVH).
Subjects And Methods: A total of 647 patients (347 females and 300 males) with newly diagnosed mild to moderate essential hypertension were enrolled in a blood pressure matched, case-control study.
Our previous study showed that epigallocatechin-3-gallate (EGCG) inhibition of human aortic smooth muscle cell (HASMC) proliferation might be mediated via upregulation of mitofusin 2 (Mfn-2). Studies on the mechanism of Mfn-2 inhibition of cell proliferation have mainly focused on downstream signaling. However, it is still not clear how upstream signaling molecules regulate Mfn-2.
View Article and Find Full Text PDFBackground: Several studies have revealed that high shock index (SI) is a risk factor for acute myocardial infarction (AMI) patients. These studies do not give a systematic review in this issue. Therefore, we conducted a systematic review and meta-analysis to determine the effect of high SI on the prognosis of AMI patients.
View Article and Find Full Text PDFPrevious studies have shown that epigallocatechin-3-gallate (EGCG) inhibits the proliferation of vascular smooth muscle cells (VSMCs) via the extracellular-signal-regulated kinase (ERK1/2) and mitogen activated protein kinases (MAPKs) pathway. Mitofusin 2 (Mfn-2) also suppresses VSMC proliferation through Ras-Raf-ERK/MAPK, suggesting a possible link between EGCG, Mfn-2 and ERK/MAPK. However, the effect of EGCG on Mfn-2 remains unknown.
View Article and Find Full Text PDFCell Biochem Biophys
November 2014
Recent studies have shown that endothelial progenitor cells (EPCs) participated in angiogenic effects of nicotine and nicotine dose dependently increased the functional activity of early EPCs. The effects of nicotine on late EPCs remain to be determined. Therefore, we investigated whether nicotine had influences on the functional activity of late EPCs.
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