Search Results (16)

Background/Objectives: MicroRNAs (miRNAs) have emerged as molecular mediators involved in the pathogenesis of rheumatoid arthritis (RA). Given the influence of diet on gene expression and inflammation, plant-based diets represent a potential non-pharmacological strategy for modulating disease activity. This study aimed to explore and validate, through a bioinformatic-guided pilot approach, the regulation of miRNAs associated with RA in response to a 14-day plant-based dietary intervention. Methods: Candidate miRNAs were identified through differential expression analysis of the GSE124373 dataset using GEO2R and were further supported by a literature review. Target gene prediction and functional enrichment analyses were conducted to assess the biological relevance of these findings. Twenty-three RA patients followed a plant-based diet for 14 days. The clinical activity (DAS28-CRP), biochemical markers, and plasma expression of five selected miRNAs (miR-26a-5p, miR-125a-5p, miR-125b-5p, miR-146a-5p, and miR-155-5p) were evaluated before and after the intervention using RT-qPCR. Results: Significant reductions were observed in DAS28-CRP scores, C-reactive protein, glucose, and lipid levels after 14 days of intervention. Three of the five miRNAs (miR-26a-5p, miR-125a-5p, and miR-155-5p) were significantly downregulated post-intervention. Bioinformatic analyses indicated that these miRNAs regulate immune–inflammatory pathways relevant to RA pathogenesis. Conclusions: This pilot study suggests that a short-term plant-based dietary intervention may modulate circulating miRNAs and improve clinical and biochemical parameters in RA patients. These findings support further research into dietary strategies as complementary approaches for RA management. Full article

Background/Objectives: RA is a chronic autoimmune disease characterized by systemic inflammation and progressive joint damage. Plant-based dietary interventions have recently emerged as complementary anti-inflammatory therapy for active RA. However, the molecular anti-inflammatory mechanisms of plant-based dietary patterns in these patients are still poorly understood. Long non-coding RNAs (lncRNAs) have emerged as key regulators of inflammation in chronic diseases. Thus, this study aimed to evaluate the expression of lncRNAs and inflammatory genes in relation to the clinical response to following a plant-based dietary intervention in patients with active RA. Methods: A two-phase whole-blood gene expression analysis was conducted for patients with active RA before and after a 14-day plant-based dietary intervention. In the discovery phase, seven patients showing the greatest reduction in disease activity (DAS28-CRP) were selected, and the expression of 84 inflammatory genes and 84 lncRNAs was analyzed using RT² Profiler PCR Array platforms. In the validation phase, by adding 14 patients, we assessed 21 participants. Results: NUTM2A-AS1 was the only significantly overexpressed lncRNA in the discovery phase (p = 0.0435), while CCR3 was the only inflammatory gene showing significant expression change (p = 0.0156). In the validation phase, both NUTM2A-AS1 and CCR3 maintained the same pattern of overexpression, confirming their modulation after the 14-day plant-based dietary intervention (p = 0.0131 and p < 0.001, respectively). Conclusions: This study showed that a 14-day plant-based diet was sufficient to modify the inflammatory circuits in patients with active RA, suggesting a potential dietary-mediated inflammatory modulation mechanism involving NUTM2A-AS1 and CCR3. Further studies are required to validate new hypotheses on the biological significance of the regulation of these transcripts and its clinical implications in RA management. Full article

Background/Objectives: Aortic stenosis (AS) is the most prevalent valvular disease among older adults. Although obstructive sleep apnea (OSA) has been linked to adverse cardiovascular outcomes, its specific impact on patients with severe AS remains unclear. This study aimed to determine the prevalence of OSA and its influence on postoperative recovery following aortic valve replacement. Methods: A prospective case-control study was conducted at the Instituto Nacional de Cardiología Ignacio Chávez. Patients aged 40–80 years with echocardiographically confirmed severe AS were categorized into groups with and without OSA, based on respiratory polygraphy (Apnea–Hypopnea Index [AHI] threshold of >15 events per hour). Clinical, biochemical, echocardiographic, body composition, and hemodynamic parameters were assessed. Daytime sleepiness and sleep quality were evaluated using validated questionnaires. Inflammatory biomarkers were also analyzed. This study was approved by the institutional ethics committee. Results: Of the 30 patients included, 66.6% were diagnosed with OSA. Compared to non-OSA patients, those with OSA had a higher left ventricular mass index (160 vs. 108; p = 0.001), greater postoperative increases in central venous pressure [8 (8–10) vs. 8 (6–8); p = 0.037], and lower mixed venous oxygen saturation within the first 24 h (69.2 vs. 76; p = 0.027). OSA patients also had longer hospital stays (11 vs. 8 days; p = 0.014). Trends toward a heightened subclinical inflammatory state were noted in the OSA group. Conclusions: OSA is frequent and underdiagnosed in patients with severe AS and is associated with more complicated postoperative recovery. Systematic OSA screening is recommended for candidates undergoing aortic valve surgery. Full article

Background/Objectives: Uric acid is a key metabolic byproduct of purine degradation and plays a dual role in human health. At physiological levels, it acts as an antioxidant, protecting against oxidative stress. However, excessive uric acid can lead to hyperuricemia, contributing to conditions like gout, kidney stones, and cardiovascular diseases. Emerging evidence also links elevated uric acid levels with metabolic disorders, including hypertension and insulin resistance. Understanding its regulation is crucial for preventing associated health complications. Methods: This study, part of the Tlalpan 2020 project, aimed to predict uric acid levels using advanced machine learning algorithms. The dataset included clinical, anthropometric, lifestyle, and nutritional characteristics from a cohort in Mexico City. We applied Boosted Decision Trees (Boosted DTR), eXtreme Gradient Boosting (XGBoost), Categorical Boosting (CatBoost), and Shapley Additive Explanations (SHAP) to identify the most relevant variables associated with hyperuricemia. Feature engineering techniques improved model performance, evaluated using Mean Squared Error (MSE), Root-Mean-Square Error (RMSE), and the coefficient of determination (R²). Results: Our study showed that XGBoost had the highest accuracy for anthropometric and clinical predictors, while CatBoost was the most effective at identifying nutritional risk factors. Distinct predictive profiles were observed between men and women. In men, uric acid levels were primarily influenced by renal function markers, lipid profiles, and hereditary predisposition to hyperuricemia, particularly paternal gout and diabetes. Diets rich in processed meats, high-fructose foods, and sugary drinks showed stronger associations with elevated uric acid levels. In women, metabolic and cardiovascular markers, family history of metabolic disorders, and lifestyle factors such as passive smoking and sleep quality were the main contributors. Additionally, while carbohydrate intake was more strongly associated with uric acid levels in women, fructose and sugary beverages had a greater impact in men. To enhance model robustness, a cross-feature selection approach was applied, integrating top features from multiple models, which further improved predictive accuracy, particularly in gender-specific analyses. Conclusions: These findings provide insights into the metabolic, nutritional characteristics, and lifestyle determinants of uric acid levels, supporting targeted public health strategies for hyperuricemia prevention. Full article

Background/Objectives: A well-established association exists between the development of hypertension and sleep quality. The connection between self-reported sleep quality and the onset of hypertension is particularly significant in populations with metabolic deterioration, such as in Mexico. Methods: The Tlalpan 2020 Cohort was analyzed to explore this association. Clinical and anthropometric characteristics, along with the Medical Outcomes Study Sleep Scale (MOS-SS), were compared between participants who developed hypertension and those who did not over a follow-up period of 30.8 months. The potential role of poor sleep quality in the development of hypertension was assessed. Results: Among 1520 participants, 12% developed hypertension. These individuals had higher anthropometric and laboratory values and reported poorer sleep quality. An elevated sleep problems index was associated with a 50% higher relative risk of developing hypertension (OR: 1.5; 95% CI: 1.087 to 2.069). Additionally, self-reported snoring was associated with hypertension onset (36.3 vs. 43.3; p = 0.019). Conclusions: Poor sleep quality and respiratory disturbances during sleep increase the risk of developing hypertension. Furthermore, hypertension was associated with snoring, highlighting the importance of early interventions to improve sleep quality. Full article

The role of ferroptosis and iron metabolism dysregulation in the pathophysiology of cardiovascular diseases is increasingly recognized. Conditions such as hypertension, cardiomyopathy, atherosclerosis, myocardial ischemia/reperfusion injury, heart failure, and cardiovascular complications associated with COVID-19 have been linked to these processes. Inflammation is central to these conditions, prompting exploration into the inflammatory and immunoregulatory molecular pathways that mediate ferroptosis and its contribution to cardiovascular disease progression. Notably, emerging evidence highlights interleukin-37 as a protective cytokine with the ability to activate the nuclear factor erythroid 2-related factor 2 pathway, inhibit macrophage ferroptosis, and attenuate atherosclerosis progression in murine models. However, a comprehensive review focusing on interleukin-37 and its protective role against ferroptosis in CVD is currently lacking. This review aims to fill this gap by summarizing existing knowledge on interleukin-37, including its regulatory functions and impact on ferroptosis in conditions such as atherosclerosis and myocardial infarction. We also explore experimental strategies and propose that targeting interleukin-37 to modulate ferroptosis presents a promising therapeutic approach for the prevention and treatment of cardiovascular diseases. Full article

This study investigated the relationship between Metabolic Syndrome (MetS), sleep disorders, the consumption of some nutrients, and social development factors, focusing on gender differences in an unbalanced dataset from a Mexico City cohort. We used data balancing techniques like SMOTE and ADASYN after employing machine learning models like random forest and RPART to predict MetS. Random forest excelled, achieving significant, balanced accuracy, indicating its robustness in predicting MetS and achieving a balanced accuracy of approximately 87%. Key predictors for men included body mass index and family history of gout, while waist circumference and glucose levels were most significant for women. In relation to diet, sleep quality, and social development, metabolic syndrome in men was associated with high lactose and carbohydrate intake, educational lag, living with a partner without marrying, and lack of durable goods, whereas in women, best predictors in these dimensions include protein, fructose, and cholesterol intake, copper metabolites, snoring, sobbing, drowsiness, sanitary adequacy, and anxiety. These findings underscore the need for personalized approaches in managing MetS and point to a promising direction for future research into the interplay between social factors, sleep disorders, and metabolic health, which mainly depend on nutrient consumption by region. Full article

An association has been suggested between acute myocardial infarction (AMI) and obstructive sleep apnea (OSA). Considering the role of adipose-tissue-derived inflammatory mediators (adipokines) and the shared risk factor of obesity in OSA and AMI, this study aimed to investigate the involvement of adipokines in AMI patients with and without OSA. Serum levels of adipokines and inflammatory mediators were quantified, and home respiratory polygraphy was conducted. A total of 30 AMI patients and 25 controls were included. Patients with AMI exhibited elevated levels of resistin (7.4 vs. 3.7 ng/mL), interleukin-6 (8.8 vs. 1.3 pg/mL), and endothelin-1 (3.31 vs. 1.8 pg/mL). Remarkably, AMI patients with concomitant OSA exhibited higher levels of resistin (7.1 vs. 3.7 ng/mL), interleukin-6 (8.9 vs. 1.3 pg/mL), endothelin-1 (3.2 vs. 1.8 pg/mL), creatin kinase (1430 vs. 377 U/L), creatine kinase-MB (64.6 vs. 9.7 ng/mL), and troponin T (2298 vs. 356 pg/mL) than their non-OSA counterparts. Leptin showed a correlation with OSA severity markers. OSA was associated with greater cardiac damage in AMI patients. Our findings underscore that adipokines alone are not sufficient to discriminate the risk of AMI in the presence of OSA. Further research is necessary to determine the potential mechanisms contributing to exacerbated cardiac damage in patients with both conditions. Full article

COVID-19, a disease caused by the SARS-CoV-2 virus, poses significant threats to the respiratory system and other vital organs. Long non-coding RNAs have emerged as influential epigenetic regulators and promising biomarkers in respiratory ailments. The objective of this study was to identify candidate lncRNAs in SARS-CoV-2-positive individuals compared to SARS-CoV-2-negative individuals and investigate their potential association with ARDS-CoV-2 (acute respiratory distress syndrome). Employing qRT-PCR, we meticulously examined the expression profiles of a panel comprising 84 inflammation-related lncRNAs in individuals presenting upper respiratory infection symptoms, categorizing them into those testing negative or positive for SARS-CoV-2. Notably, first-phase PSD individuals exhibited significantly elevated levels of AC000120.7 and SENP3-EIF4A1. In addition, we measured the expression of two lncRNAs, AC000120.7 and SENP3-EIF4A1, in patients with ARDS unrelated to SARS-CoV-2 (n = 5) and patients with ARDS induced by SARS-CoV-2 (ARDS-CoV-2, n = 10), and interestingly, expression was also higher among patients with ARDS. Intriguingly, our interaction pathway analysis unveiled potential interactions between lncRNA AC000120.7, various microRNAs, and genes associated with inflammation. This study found higher expression levels of lncRNAs AC000120.7 and SENP3-EIF4A1 in the context of infection-positive COVID-19, particularly within the complex landscape of ARDS. Full article

Atherosclerotic cardiovascular disease (CVD) remains the leading cause of mortality worldwide. While conventional risk factors have been studied and managed, CVD continues to pose a global threat. Risk scoring systems based on these factors have been developed to predict acute coronary syndromes and guide therapeutic interventions. However, traditional risk algorithms may not fully capture the complexities of individual patients. Recent research highlights the role of inflammation, particularly chronic low-grade inflammation, in the pathogenesis of coronary artery disease (CAD). C-reactive protein (CRP) is an inflammatory molecule that has demonstrated value as a predictive marker for cardiovascular risk assessment, both independently and in conjunction with other parameters. It has been incorporated into risk assessment algorithms, enhancing risk prediction and guiding therapeutic decisions. Pharmacological interventions with anti-inflammatory properties, such as statins, glucagon-like peptide-1 agonists, and interleukin-1 inhibitors, have shown promising effects in reducing both cardiovascular risks and CRP levels. This manuscript provides a comprehensive review of CRP as a marker of systemic inflammation in CAD. By exploring the current knowledge surrounding CRP and its implications for risk prediction and therapeutic interventions, this review contributes to the advancement of personalized cardiology and the optimization of patient care. Full article

Prompt diagnosis of ST-segment elevation myocardial infarction (STEMI) is essential for initiating timely treatment. MicroRNAs have recently emerged as biomarkers in cardiovascular diseases. This study aimed to evaluate the discriminatory capacity of serum microRNAs in identifying an ischemic origin in patients presenting with chest discomfort to the Emergency Department. The study included 98 participants (78 with STEMI and 20 with nonischemic chest discomfort). Significant differences in the expression levels of miR-133b, miR-126, and miR-155 (but not miR-1, miR-208, and miR-208b) were observed between groups. miR-133b and miR-155 exhibited 97% and 93% sensitivity in identifying STEMI patients, respectively. miR-126 demonstrated a specificity of 90% in identifying STEMI patients. No significant associations were found between microRNAs and occurrence of major adverse cardiovascular events (MACE). However, patients with MACE had higher levels of interleukin (IL)-15, IL-21, IFN-γ-induced protein-10, and N-terminal pro B-type natriuretic peptide compared to non-MACE patients. Overall, there were significant associations among the expression levels of microRNAs. However, microRNAs did not demonstrate associations with either inflammatory markers or cardiovascular risk scores. This study highlights the potential of microRNAs, particularly miR-133b and miR-126, as diagnostic biomarkers for distinguishing patients with STEMI from those presenting with nonischemic chest discomfort to the Emergency Department. Full article

Background: Coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Clinical manifestations of COVID-19 range from mild flu-like symptoms to severe respiratory failure. Nowadays, extracellular matrix metalloproteinase inducer (EMMPRIN), also known as cluster of differentiation 147 (CD147) or BASIGIN, has been studied as enabling viral entry and replication within host cells. However, the impact of the CD147 rs8259T>A single nucleotide variant (SNV) on SARS-CoV-2 susceptibility remains poorly investigated. Objective: To investigate the impact of rs8259T>A on the CD147 gene in individuals from Mexico with COVID-19 disease. Methods: We genotyped the CD147 rs8359T>A SNV in 195 patients with COVID-19 and 185 healthy controls from Mexico. In addition, we also measured the expression levels of CD147 and TNF mRNA and miR-492 from whole blood of patients with COVID-19 through RT-q-PCR. Results: We observed a significant association between the CD147 rs8259T>A SNV and susceptibility to COVID-19: T vs. A; OR 1.36, 95% CI 1.02–1.81; p = 0.037; and TT vs. AA; OR 1.77, 95% CI 1.01–3.09; p = 0.046. On the other hand, we did not find differences in CD147, TNF or miR-492 expression levels when considering the genotypes of the CD147 rs8259T>A SNV. Conclusions: Our results suggest that the CD147 rs8259T>A variant is a risk factor for COVID-19. Full article

Trimethylamine N-oxide (TMAO) is a metabolite produced by the gut microbiota and has been mainly associated with an increased incidence of cardiovascular diseases (CVDs) in humans. There are factors that affect one’s TMAO level, such as diet, drugs, age, and hormones, among others. Gut dysbiosis in the host has been studied recently as a new approach to understanding chronic inflammatory and degenerative diseases, including cardiovascular diseases, metabolic diseases, and Alzheimer’s disease. These disease types as well as COVID-19 are known to modulate host immunity. Diabetic and obese patients have been observed to have an increase in their level of TMAO, which has a direct correlation with CVDs. This metabolite is attributed to enhancing the inflammatory pathways through cholesterol and bile acid dysregulation, promoting foam cell formation. Additionally, TMAO activates the transcription factor NF-κB, which, in turn, triggers cytokine production. The result can be an exaggerated inflammatory response capable of inducing endoplasmic reticulum stress, which is responsible for various diseases. Due to the deleterious effects that this metabolite causes in its host, it is important to search for new therapeutic agents that allow a reduction in the TMAO levels of patients and that, thus, allow patients to be able to avoid a severe cardiovascular event. The present review discussed the synthesis of TMAO and its contribution to the pathogenesis of various inflammatory diseases. Full article

In the modern diet, excessive fructose intake (>50 g/day) had been driven by the increase, in recent decades, of the consumption of sugar-sweetened beverages. This phenomenon has dramatically increased within the Caribbean and Latin American regions. Epidemiological studies show that chronic high intake of fructose related to sugar-sweetened beverages increases the risk of developing several non-communicable diseases, such as chronic obstructive pulmonary disease and asthma, and may also contribute to the exacerbation of lung diseases, such as COVID-19. Evidence supports several mechanisms—such as dysregulation of the renin–angiotensin system, increased uric acid production, induction of aldose reductase activity, production of advanced glycation end-products, and activation of the mTORC1 pathway—that can be implicated in lung damage. This review addresses how these pathophysiologic and molecular mechanisms may explain the lung damage resulting from high intake of fructose. Full article

Background: Several easy-to-use risk scoring systems have been built to identify patients at risk of developing complications associated with COVID-19. However, information about the ability of each score to early predict major adverse outcomes during hospitalization of severe COVID-19 patients is still scarce. Methods: Eight risk scoring systems were rated upon arrival at the Emergency Department, and the occurrence of thrombosis, need for mechanical ventilation, death, and a composite that included all major adverse outcomes were assessed during the hospital stay. The clinical performance of each risk scoring system was evaluated to predict each major outcome. Finally, the diagnostic characteristics of the risk scoring system that showed the best performance for each major outcome were obtained. Results: One hundred and fifty-seven adult patients (55 ± 12 years, 66% men) were assessed at admission to the Emergency Department and included in the study. A total of 96 patients (61%) had at least one major outcome during hospitalization; 32 had thrombosis (20%), 80 required mechanical ventilation (50%), and 52 eventually died (33%). Of all the scores, Obesity and Diabetes (based on a history of comorbid conditions) showed the best performance for predicting mechanical ventilation (area under the ROC curve (AUC), 0.96; positive likelihood ratio (LR+), 23.7), death (AUC, 0.86; LR+, 4.6), and the composite outcome (AUC, 0.89; LR+, 15.6). Meanwhile, the inflammation-based risk scoring system (including leukocyte count, albumin, and C-reactive protein levels) was the best at predicting thrombosis (AUC, 0.63; LR+, 2.0). Conclusions: Both the Obesity and Diabetes score and the inflammation-based risk scoring system appeared to be efficient enough to be integrated into the evaluation of COVID-19 patients upon arrival at the Emergency Department. Full article