Reports of Biochemistry

Background: MicroRNA expression signature and reactive oxygen species (ROS) production have been associated with the development of cardiovascular diseases (CVDs). This study aimed to evaluate oxidative stress, inflammation, apoptosis, and the expression of miRNA-208a and miRNA-1 in cardiovascular patients.

Methods: The study population included four types of patients (acute coronary syndromes (ACS), myocardial infarction (MI), arrhythmia, and heart failure (HF)), with 10 people in each group, as well as a control group. Quantitative real-time PCR was performed to measure mir-208 and miR-1 expression, the mRNAs of inflammatory mediators (TNFα, iNOS/eNOS), and apoptotic factors (Bax and Bcl2). XOX, MDA, and antioxidant enzymes (CAT, SOD, and GPx) were measured by ZellBio GmbH kits by an ELISA Reader.

Results: The results showed significant decreases in the activity of antioxidant enzymes (CAT, SOD, and Gpx) and a significant increase in the activity of the MDA and XOX in cardiovascular patients. Significant increases in IL-10, iNos, iNOS / eNOS, and TNF-α in cardiovascular patients were also observed. Also, a significant increase in the expression of miR-208 (HF> arrhythmia> ACS> MI) and a significant decrease in the expression of miR-1 (ACS> arrhythmia> HF> MI) were found in all four groups in cardiovascular patients.

Conclusions: The results showed increases in oxidative stress, inflammation, apoptotic factors, and in the expression of miR-208a in a variety of cardiovascular patients (ACS, MI, arrhythmia, and HF). It is suggested that future studies determine the relationships that miR-1, miR-208, and oxidative stress indices have with inflammation and apoptosis.

Background: Cardiovascular disease is one of the most common causes of morbidity and mortality worldwide. The Proline and Serine Rich Coiled-Coil 1 gene in 1p13.3 locus has been reported to be associated with low density lipoprotein cholesterol (LDL-C) and coronary artery disease (CAD). The objective of this study was to investigate the association between the rs599839 polymorphism of the Proline and Serine Rich Coiled-Coil 1 (PSRC1) gene with CVD outcomes in a population sample recruited as part of the Mashhad-Stroke and Heart-Atherosclerotic-Disorders (MASHAD) cohort.

Methods: Five hundred and nine individuals who had an average follow-up period of 10 years were enrolled as part of the MASHAD cohort. DNA was extracted and genotyped using the TaqMan-real-time-PCR based method.

Results: The study found individuals with GA/GG genotypes were at a higher risk of CVDs (OR= 4.7; 95% CI, 2.5-8.7; p< 0.001) in comparison to those with AA genotype; however, the result was not significant for GG genotype data.

Conclusions: The results suggest that the GA/GG genotypes of the PSRC1gene locus were at increased risk of CVD in a representative population-based cohort, demonstrating further functional analysis to discover the value of emerging marker as a risk stratification biomarker to recognize high risk cases.

Background: Globally, cardiovascular diseases (CVDs) are the leading cause of death and disability. Elevated low-density lipoprotein-cholesterol (LDL-C) and more specifically, elevation of its small, dense phenotype (sdLDL-C) has been regarded as the key modifiable risk factors associated with atherogenesis. This study aimed to determine the association of LDL-C and sdLDL-C with the development of CVDs in the next six months to establish their predictive efficacy.
 

had the greatest correlation.
 

Results: Four control group patients and three test group patients developed the outcome (any cardiovascular event) during the 6-month follow-up period. Binary logistic regression analysis showed that none of the lipid profile parameters: calculated LDL-C (OR= 0.99; 95% CI= 0.97-1.01; p= 0.826), direct LDL-C (OR= 0.99; 95% CI= 0.97-1.01; p= 0.818) or sdLDL-C (OR= 0.99; 95% CI= 0.93-1.04; p= 0.734), were significantly associated with the occurrence of outcome. The median % sdLDL-C both with respect to direct and calculated LDL-C was slightly higher in patients with the outcome.
 

Background: Preeclampsia (PE) is a serious multisystem disorder that ranks among the leading causes of maternal and neonatal morbidity and mortality. The condition is characterized by an angiogenic imbalance, which has adverse effects on fetal development and contributes to an increased risk of cardiovascular disease in the long term. This study aims to explore the connection between sterile inflammation mediated by HMGB1 and angiogenic imbalance in PE by examining key markers such as HMGB1, VEGF, Decorin, and TGF-β.

Methods: In an animal model of PE, we measured the levels of HMGB1, VEGF, Decorin, and TGF-β in plasma, placenta, and heart tissues using ELISA. Additionally, Decorin levels were assessed through immunofluorescence in trophoblasts.

Results: We found that levels of Decorin and TGF-β were significantly elevated in the plasma, placenta, and heart tissues of PE animals compared to non-pregnant and pregnant controls, whereas VEGF levels were reduced. Treatment with Glycyrrhizic acid (GA) restored the expression levels of these markers to more normalized values in the PE groups.

Conclusion: Our findings indicate that HMGB1 plays a critical role in preeclampsia by mediating the upregulation of anti-angiogenic factors like Decorin and the downregulation of angiogenic factors like VEGF. This study highlights a significant correlation between HMGB1 and Decorin in driving the angiogenic imbalance that contributes to the pathophysiology of PE.