Etiology Of Cardiovascular Disease Research Articles

Eating jetlag and risk of cardiovascular disease: prospective study of the NutriNet-Santé cohort

Abstract Background Social jetlag corresponds to the misalignment between biological circadian rhythms and the social rhythm imposed by society, resulting in discrepant activity/sleep schedules during work and free days. It has been associated with worsened biological parameters such as BMI or glycemic control. Eating jetlag is a related yet emerging concept defined as the difference of meal timing between free and work days. However, it has been little explored. This study aims to evaluate the association between eating jetlag and the risk of cardiovascular disease (CVD). Methods Dietary, anthropometric, socio-demographic and health data of 104,837 participants (79% women, mean age=42.7 years (14.6 SD)) were collected from the NutriNet-Santé cohort. Eating jetlag was calculated using time of first and last meals on weekdays and weekends, from repeated 24 dietary records, averaged during the 2 first years. It was assessed as a continuous variable or as 3 categories: ‘Advance’, ‘Maintenance’, ‘Delay’, compared to work days. CVD was self-reported and validated against medical records. The associations between eating jetlag and CVD risk were assessed through adjusted Cox models. Results During a median follow-up time of 8.1 years, 2,368 CVD cases were diagnosed. Eating jetlag showed a U-shaped association with CVD risk (HR Advance vs. Maintenance=1.05(95% CI: 0.87-1.26); HR Delay vs. Maintenance=1.08(0.96-1.21)). When the absolute value of eating jetlag was considered, there was a linear association with CVD risk (HR per 1-hour increase=1.05(1.00-1.12)). These linear trends were confirmed in categorial models (Low: ≤1h; Moderate: 1h< to ≤ 2h; High: >2h): HR Moderate vs. Low=1.05(0.94-1.18), and HR High vs. Low=1.13(0.94-1.37); however, statistical significance was not reached. Conclusions Our results suggest a potential role for meal timing regularity between free and work days in CVD etiology. They need to be replicated in other studies and mechanisms are yet to be fully understood. Key messages • Adopting regular meal timing schemes on work and free days could be associated with a lower risk of cardiovascular diseases. • Meal regularity between work and free days could play a role in cardiovascular health and should be further investigated.

Genome-wide association study of CMR image-based aortic stiffness in 45,789 individuals identifies loci linked with cardiovascular diseases

Abstract Background The use of artificial intelligence on large-scale cardiac magnetic resonance (CMR) imaging data has enabled detailed characterisation of cardiac shape and function for use in genome-wide association studies (GWAS), leading to improved understanding of genetic aetiology of cardiovascular diseases (CVDs). Aortic stiffness is associated with increased risk of cardiovascular events in observational studies. Here, we present a novel CMR-based pressure-independent measure of aortic stiffness, identify genetic associations and explore links with CVDs. Purpose Identify genetic contributions to pressure-independent aortic stiffness and links to CVDs using large-scale GWAS analysis on the UK Biobank cohort. Methods A pre-trained neural network was used to segment CMR images of participants in the UK Biobank to quantify ascending aorta diameter, which together with contemporaneous systolic and diastolic blood pressure measurements (SBP, DBP, respectively) were used to calculate a pressure-independent measure of aortic stiffness (β0). The measurement assumes an exponential relationship between pressure and aortic diameter. We then performed a GWAS on β0 in 45,789 participants of European ancestry without CVDs. A multi-trait-based conditional & joint analysis (mtCOJO) was performed to estimate genetic effects independent of SBP, DBP and aortic area. We mapped the independent lead variants associated with aortic stiffness at P < 5x10-8 to nearest gene, and characterised shared genetic association across CVDs using Open Targets Platform database. Results The GWAS identified 17 independent lead variants, including 6 that remained significant in the conditional analysis. Four of these lead variants, not previously reported in GWAS of other aortic traits, were located near CTD-2203A3.1, MCF2L, CFDP1 and CDH13 genes (red annotations in the Figure). MCF2L, CFDP1 and CDH13 have been associated with coronary artery disease, and CFDP1 with myocardial infarction and coronary atherosclerosis in previous studies. Conclusion A GWAS of CMR-derived aortic stiffness identified 4 loci distinct from other aortic traits that also associate with other CVDs, suggesting genetic links between aortic stiffness and CVDs. Further analyses are required to explore biological mechanisms underlying these genetic associations.Aortic Stiffness Manhattan Plot

Alcohol Consumption and Cardiovascular Disease: A Narrative Review of Evolving Perspectives and Long-Term Implications.

Cardiovascular illnesses remain the primary cause of death, accounting for at least 17.9 million fatalities per year and posing a significant public health problem because of its extensive predominance and effect on healthcare systems. The etiology of cardiovascular disease is complex and involves several environmental and lifestyle factors. Alcohol use is a highly important determinant because of its dual-edged effect on cardiovascular health. Multiple studies indicate that moderate alcohol consumption may have certain advantages, such as slight enhancements in lipid profiles. Conversely, excessive alcohol intake is associated with serious negative consequences, including cardiomyopathy, hypertension, arrhythmias, and even mortality. The aim of this study is to provide a comprehensive analysis of the several effects of alcohol on cardiovascular health and their understanding within the medical field over time. It uses an interpretative narrative review methodology and analyzes studies that focus on genetic risk factors, gender differences, and shifts in paradigms in recent years. This article highlights the need for obtaining a thorough understanding of the effects of alcohol on cardiovascular health to support public health guidelines and clinical practice, and it underscores the significance of including alcohol consumption into the broader context of cardiovascular risk management and identifies important subjects for further study.

Effect of vitamin D deficiency on uric acid/HDL cholesterol ratio

Aims: It has been suggested that vitamin D deficiency is involved in the etiology of cardiovascular diseases. High uric acid and low HDL cholesterol levels are critical risk factors for cardiovascular diseases. High uric acid levels, high total cholesterol and triglyceride levels, and low HDL-C levels are often encountered in cases with vitamin D deficiency. Our study aimed to investigate the relationship between vitamin D levels and uric acid /HDL-C (UHR) and plasma atherogenic index (PAI, triglyceride /HDL-C) in patients with vitamin D deficiency. Methods: This retrospective study included patients whose vitamin D levels were checked in our clinic. The subjects were divided into two groups according to their vitamin D levels and the relationship between laboratory variables, such as uric acid, HDL cholesterol, UHR, and plasma atherogenic index, was examined. Results: A total of 675 patients, 167 (24.7%) males and 508 (75.3%) females, were included in the study. The mean age of the patients was 53.6±15.2 years. It was found that patients with vitamin D deficiency had high UHR and PAI levels and low HDL-C levels (p=0.001, p=0.025; p=0.032, p=0.016). Conclusion Our results suggest that vitamin D deficiency has a positive correlation with HDL cholesterol levels and an impact on the risk of cardiovascular diseases by increasing the uric acid/HDL ratio and plasma atherogenic index.

Cardiovascular disease risk: it is complicated, but race and ethnicity are key, a Bayesian network analysis.

Cardiovascular diseases are the leading cause of morbidity and mortality in the United States. Despite the complexity of cardiovascular disease etiology, we do not fully comprehend the interactions between non-modifiable factors (e.g., age, sex, and race) and modifiable risk factors (e.g., health behaviors and occupational exposures). We examined proximal and distal drivers of cardiovascular disease and elucidated the interactions between modifiable and non-modifiable risk factors. We used a machine learning approach on four cohorts (2005-2012) of the National Health and Nutrition Examination Survey data to examine the effects of risk factors on cardiovascular risk quantified by the Framingham Risk Score (FRS) and the Pooled Cohort Equations (PCE). We estimated a network of risk factors, computed their strength centrality, closeness, and betweenness centrality, and computed a Bayesian network embodied in a directed acyclic graph. In addition to traditional factors such as body mass index and physical activity, race and ethnicity and exposure to heavy metals are the most adjacent drivers of PCE. In addition to the factors directly affecting PCE, sleep complaints had an immediate adverse effect on FRS. Exposure to heavy metals is the link between race and ethnicity and FRS. Heavy metal exposures and race/ethnicity have similar proximal effects on cardiovascular disease risk as traditional clinical and lifestyle risk factors, such as physical activity and body mass. Our findings support the inclusion of diverse racial and ethnic groups in all cardiovascular research and the consideration of the social environment in clinical decision-making.

Blockade of endothelial adenosine receptor 2 A suppresses atherosclerosis in vivo through inhibiting CREB-ALK5-mediated endothelial to mesenchymal transition

Cardiovascular diseases (CVDs) are the leading cause of death worldwide, and morbidity and mortality rates continue to rise. Atherosclerosis constitutes the principal etiology of CVDs. Endothelial injury, inflammation, and dysfunction are the initiating factors of atherosclerosis. Recently, we reported that endothelial adenosine receptor 2 A (ADORA2A), a G protein-coupled receptor (GPCR), plays critical roles in neovascularization disease and cerebrovascular disease. However, the precise role of endothelial ADORA2A in atherosclerosis is still not fully understood. Here, we showed that ADORA2A expression was markedly increased in the aortic endothelium of humans with atherosclerosis or Apoe-/- mice fed a high-cholesterol diet. In vivo studies unraveled that endothelial-specific Adora2a deficiency alleviated endothelial-to-mesenchymal transition (EndMT) and prevented the formation and instability of atherosclerotic plaque in Apoe-/- mice. Moreover, pharmacologic inhibition of ADORA2A with KW6002 recapitulated the anti-atherogenic phenotypes observed in genetically Adora2a-deficient mice. In cultured human aortic endothelial cells (HAECs), siRNA knockdown of ADORA2A or KW6002 inhibition of ADORA2A decreased EndMT, whereas adenoviral overexpression of ADORA2A induced EndMT. Mechanistically, ADORA2A upregulated ALK5 expression via a cAMP/PKA/CREB axis, leading to TGFβ-Smad2/3 signaling activation, thereby promoting EndMT. In conclusion, these findings, for the first time, demonstrate that blockade of ADORA2A attenuated atherosclerosis via inhibition of EndMT induced by the CREB1-ALK5 axis. This study discloses a new link between endothelial ADORA2A and EndMT and indicates that inhibiting endothelial ADORA2A could be an effective novel strategy for the prevention and treatment of atherosclerotic CVDs.

Atherogenic Index as a Cardiovascular Biomarker in Mexican Workers from Marginalized Urban Areas Occupationally Exposed to Metals

Cardiovascular disease (CVD) is one of the main causes of death and disability worldwide. The etiology of CVD is often associated with multiple risk factors, with environmental factors receiving considerable attention. Individuals with precarious jobs are among the groups most affected by chronic exposure to environmental pollutants. This study aimed to evaluate occupational exposure to heavy metals among individuals in precarious job settings and investigate atherogenic indices as biomarkers of cardiovascular risk. A total of 137 workers participated in this cross-sectional study conducted in three work environments in San Luis Potosi, Mexico. Urine and blood samples were collected to assess metal exposure and biochemical profiles, including atherogenic indices. The results showed that workers in the brick sector exhibited the highest levels of metal exposure, particularly arsenic (44.06 µg/L), followed by stonecutters and garbage collectors (24.7 and 16.9 µg/L, respectively). Similarly, Castelli risk index (CRI) and the atherogenic index of plasma (AIP) were higher in brickmakers (3.883 and 0.499) compared to stonecutters (3.285 and 0.386) and garbage collectors (3.329 and 0.367). Evidence of exposure to heavy metals was observed in the three populations, in addition to the fact that individuals with greater exposure to arsenic also exhibited higher CRI and AIP.

Role of the intestinal microbiome and its therapeutic intervention in cardiovascular disorder.

The gut microbiome is a heterogeneous population of microbes comprising viruses, bacteria, fungi, and protozoa. Such a microbiome is essential for sustaining host equilibrium, and its impact on human health can be altered by a variety of factors such as external variables, social behavior, age, nutrition, and genetics. Gut microbes' imbalances are related to a variety of chronic diseases including cancer, obesity, and digestive disorders. Globally, recent findings show that intestinal microbes have a significant role in the formation of cardiovascular disease (CVD), which is still the primary cause of fatalities. Atherosclerosis, hypertension, diabetes, inflammation, and some inherited variables are all cardiovascular risk variables. However, studies found correlations between metabolism, intestinal flora, and dietary intake. Variations in the diversity of gut microbes and changes in their activity are thought to influence CVD etiology. Furthermore, the gut microbiota acts as an endocrine organ, producing bioactive metabolites such as TMA (trimethylamine)/TMAO (trimethylamine N-oxide), SCFA (short-chain fatty acids), and bile acids, which have a substantial impact on host wellness and disease by multiple mechanisms. The purpose of this overview is to compile current evidence highlighting the intricate links between gut microbiota, metabolites, and the development of CVD. It focuses on how intestinal dysbiosis promotes CVD risk factors such as heart failure, hypertension, and atherosclerosis. This review explores the normal physiology of intestinal microbes and potential techniques for targeting gut bacteria for CVD treatment using various microbial metabolites. It also examines the significance of gut bacteria in disease treatment, including supplements, prebiotics, probiotics, antibiotic therapies, and fecal transplantation, which is an innovative approach to the management of CVD. As a result, gut bacteria and metabolic pathways become increasingly attractive as potential targets for CVD intervention.

Does perceived caloric and nutrient intake influence the acute effect of beverage consumption on cardiovascular function?

Our objective was to explore whether consuming the same high-fat/sugar beverage affects endothelial function differently depending on whether it is presented as "unhealthy" [accurate high calorie (kcal), fat, and sugar information displayed] versus "healthy" (inaccurate low kcal, fat, and sugar information displayed). Twenty-five, young (21 ± 2 yr), healthy, food-stress/shame-prone women completed three conditions: milkshake consumption (540 kcal, 80 g sugar, and 14 g fat) where correct, "unhealthy" nutritional information was shown to participants (milkshake condition), consumption of the same milkshake but with incorrect, "healthy" information shown to participants (100 kcal, 3 g sugar, and 4 g fat; sham-nutrishake condition), and water consumption (control condition). Pre- and postbeverage we assessed 1) endothelial function via standard brachial artery flow-mediated dilation (FMD); 2) perceived shame, stress, beverage healthiness, and harm; and 3) blood (plasma) glucose, insulin, triglycerides and oral fluid cortisol, and tumor necrosis factor-alpha (TNFα) receptor binding. Glucose, triglycerides, and insulin increased in the milkshake and sham-nutrishake conditions (P < 0.05). The milkshake was perceived as less healthy (P < 0.001) and more harmful (P < 0.001) than the sham-nutrishake. Shame, stress, oral fluid cortisol and TNFα receptor binding did not increase postconsumption. FMD decreased after the milkshake condition (pre: 7.4 ± 3.3%; post-60 min: 4.9 ± 2.9%; post-90 min: 4.5 ± 3.1%, P < 0.001) but not the sham-nutrishake (pre: 5.7 ± 2.2%; post-60 min: 5.5 ± 2.6%; post-90 min: 5.0 ± 2.4%, P = 0.43) or control conditions (pre: 7.0 ± 2.6%; post-60 min: 6.6 ± 4.1%; post-90 min: 6.0 ± 3.2%, P = 0.29). Shear rate stimulus covariation did not alter FMD results. Lower perceived beverage healthiness was significantly associated with a greater reduction in FMD (ρ = 0.36, P = 0.002). In conclusion, a high-fat/sugar milkshake reduced FMD only when presented as high in fat, sugar, and calories. This suggests that perceptions about nutritional information contribute to the impact of food intake on endothelial function and that nocebo effects could be involved in cardiovascular disease etiology.NEW & NOTEWORTHY This was the first study to investigate how perceived nutritional content influences the impact of a high-sugar/fat beverage on endothelial function. We found that a high-sugar/fat beverage only reduced endothelial function when it was presented to participants as high in calories, fat, and sugar. This suggests that perceived nutritional information contributes to the impact of high sugar and fat intake on endothelial function.

Effects of catfish oil and Curcuma longa L. extract on ApoB levels and atherosclerosis risk indicators in metabolic syndrome rats

The increase in ApoB levels, atherogenic index of plasma (AIP) and castelli risk index I-II (CRI) is prediction of cardiovascular disease in metabolic syndrome. Lipid peroxidation could initiate the process of atherosclerosis and involved in the etiology of cardiovascular disease. Dietary fish oil and extract of Curcuma has been shown to beneficially reducing effect of atherosclerosis and lipid peroxidation. The aim of this study was to determine the effect of Catfish Oil and Curcuma longa Linn extract on ApoB levels and lipid ratios as protective nutraceutical for metabolic syndrome. Thirty male Wistar rats were randomly divided into 5 groups namely HC (healthy control), HFFD (High-Fat High-Fructose Diet), and intervention group P1 (High-Fat High-Fructose Diet + Catfish Oil 0.08 ml/gr/day), P2 (High-Fat High-Fructose Diet + Curcuma longa linn extract 5.04 mg/gr/day), and P3 with High-Fat High-Fructose Diet + combination of both. HFFD was used to induced metabolic syndrome. ApoB levels were measured by the Immunoturbidimetric and lipid levels with ELISA method. Lipid ratios was calculated by AIP (log TG/HDL), and the CRI I-II (TC/HDL,LDL/HDL). The study was showed significantly reduced (p=&lt;0.05) the ApoB levels, AIP and CRI in intervention group. The coefficient value was showed that every increase in ApoB levels against AIP and CRI there was an increase of 35.309mg/dl. In conclusion, combination of both may decrease levels of ApoB, and atherosclerosis risk indicators in metabolic syndrome rats.

The importance of LDL-cholesterol and infection in the etiology of cardiovascular disease: a meta-analysis of COVID-19 survivors and non-survivors

The importance of LDL-cholesterol and infection in the etiology of cardiovascular disease: a meta-analysis of COVID-19 survivors and non-survivors

The importance of LDL-cholesterol and infection in the etiology of cardiovascular disease: a meta-analysis of COVID-19 survivors and non-survivors

The importance of LDL-cholesterol and infection in the etiology of cardiovascular disease: a meta-analysis of COVID-19 survivors and non-survivors

The Effects of Xanthine Oxidase Inhibitors on the Management of Cardiovascular Diseases

The Effects of Xanthine Oxidase Inhibitors on the Management of Cardiovascular Diseases

Central stress pathways in the development of cardiovascular disease.

Mental stress is of essential consideration when assessing cardiovascular pathophysiology in all patient populations. Substantial evidence indicates associations among stress, cardiovascular disease and aberrant brain-body communication. However, our understanding of the flow of stress information in humans, is limited, despite the crucial insights this area may offer into future therapeutic targets for clinical intervention. Key terms including mental stress, cardiovascular disease and central control, were searched in PubMed, ScienceDirect and Scopus databases. Articles indicative of heart rate and blood pressure regulation, or central control of cardiovascular disease through direct neural innervation of the cardiac, splanchnic and vascular regions were included. Focus on human neuroimaging research and the flow of stress information is described, before brain-body connectivity, via pre-motor brainstem intermediates is discussed. Lastly, we review current understandings of pathophysiological stress and cardiovascular disease aetiology. Structural and functional changes to corticolimbic circuitry encode stress information, integrated by the hypothalamus and amygdala. Pre-autonomic brain-body relays to brainstem and spinal cord nuclei establish dysautonomia and lead to alterations in baroreflex functioning, firing of the sympathetic fibres, cellular reuptake of norepinephrine and withdrawal of the parasympathetic reflex. The combined result is profoundly adrenergic and increases the likelihood of cardiac myopathy, arrhythmogenesis, coronary ischaemia, hypertension and the overall risk of future sudden stress-induced heart failure. There is undeniable support that mental stress contributes to the development of cardiovascular disease. The emerging accumulation of large-scale multimodal neuroimaging data analytics to assess this relationship promises exciting novel therapeutic targets for future cardiovascular disease detection and prevention.

Abstract 11667: Red Cell Indices and Long-Term Prognosis of Heart Failure Patients

Introduction: It has been demonstrated that some properties of red blood cells also play a role in the etiology of cardiovascular diseases and their complications. Hypothesis: We determined to what extent red blood cell indices observed during hospitalization for heart failure (HF) affect the long-term prognosis of these patients. Methods: We followed 3697 patients [mean age 71.4 years (±SD10.1), 59.1% males] hospitalized for decompensated HF between 2010-20. In the multivariate model, we assessed the five-year all-cause mortality risk associated with red cell distribution width (RDW), mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), and hemoglobin concentration (dichotomized by tertiles). Results: Kaplan-Meier survival curves comparing the tertiles of red cell indices are in Figure. Patients with RDW in the top tertile showed roughly two-fold higher 5-year mortality risk than those in the bottom tertile; increased risk we also observed in the middle tertile of RDW. This association remained significant even after complex adjustments for individual characteristics (age, gender, ejection fraction, HF etiology, history of malignancy, revascularization, hypertension, diabetes, LDL, atrial fibrillation, and glomerular filtration) as well as treatments (furosemide, beta-blockers, RAS blockers, MRA′s, statins). [HRR 1.83 (95% CIs: 1.53-2.18), p&lt;0.0001, 3 rd versus 1 st ; 1.42 (95%CIs: 1.19-1.68), p&lt;0.0001, 2 nd versus 1 st ] Similarly, we observed increased mortality risk in the bottom tertile of MCHC [HRR 1.34 (95%CIs:1.14-1.59), p=0.001, 1 st versus 3 rd ( fully adjusted)] or hemoglobin [HRR 1.37 (95%CIs: 1.15-1.62), p&lt;0.0001]. In contrast, MCV did not show any additive mortality risk. Conclusions: High degree of anisocytosis and low red cell status of hemoglobin represents independent indicators of poor prognosis in heart failure patients, even long-term after an acute manifestation.

OR07-04 Associations Of Sleep Patterns And Body Mass Index Among African Americans: The Jackson Heart Sleep Study

Abstract Disclosure: D. Duan: None. J.C. Jun: None. D.A. Johnson: None. R.S. Ahima: None. A.G. Bertoni: None. S. Redline: None. J.B. Echouffo Tcheugui: None. Background: Obesity and its metabolic complications disproportionately affect African Americans. Sleep may be a modifiable factor that can impact metabolic health. We used objective measures of sleep patterns to assess the relationship between sleep parameters and body mass index (BMI) among African Americans. Methods: The Jackson Heart Study was a prospective cohort study that recruited 5306 African American adults from 3 counties in Jackson, Mississippi, designed to evaluate the etiology of cardiovascular disease among African Americans. We performed a cross-sectional analysis including 913 participants in the Jackson Heart Sleep Ancillary Study (enrolled 2012-2016) who underwent 7-day wrist actigraphy and home sleep apnea tests. We used multivariable linear regression to assess the associations between BMI (outcome; log-transformed for normality) and actigraphy-derived sleep parameters (exposures) that described: sleep timing (sleep onset and mid-sleep time), sleep duration (total sleep duration and night to night variation measured by within-individual standard deviation), and sleep continuity (sleep maintenance efficiency and sleep fragmentation index). Models were adjusted for age, sex, socioeconomic factors, physical activity, smoking, alcohol use, and the presence of moderate to severe obstructive sleep apnea (Apnea Hypopnea Index &amp;gt; 15). Results: Among the included 684 participants with complete data on anthropometric measurements and key covariates (mean age 63 ± 11 years, 66% women, mean BMI 31.8 ± 6.9 kg/m2), average sleep onset was 23:10 ± 1.35 hrs, mid-sleep time was 2:55 ± 1.20 hrs, total sleep duration was 6.7 ± 1.15 hrs, median night-to-night variation was 1.2 hrs (IQR 0.8-1.5), median sleep maintenance efficiency was 88.9% (IQR 85.7-91.5), and median sleep fragmentation index was 28.4% (IQR 23.3-34). In adjusted models, sleep onset (β 0.013, p=0.02) and mid-sleep time (β 0.012, p=0.047) were positively associated with log transformed BMI, while sleep maintenance efficiency was negatively associated with log transformed BMI (β −0.004, p=0.009). Total sleep duration, night to night sleep duration variability, and average sleep fragmentation index were not associated with BMI in adjusted models. Conclusions: Later sleep timing and poor sleep continuity were associated with higher BMI among African Americans in the Jackson Heart Sleep Study. Our findings suggest the importance of circadian influence and sleep disruption as factors that influence metabolic health. Presentation: Thursday, June 15, 2023

The role of lncRNA-mediated pyroptosis in cardiovascular diseases.

Cardiovascular disease (CVD) is the leading cause of death worldwide. Pyroptosis is a unique kind of programmed cell death that varies from apoptosis and necrosis morphologically, mechanistically, and pathophysiologically. Long non-coding RNAs (LncRNAs) are thought to be promising biomarkers and therapeutic targets for the diagnosis and treatment of a variety of diseases, including cardiovascular disease. Recent research has demonstrated that lncRNA-mediated pyroptosis has significance in CVD and that pyroptosis-related lncRNAs may be potential targets for the prevention and treatment of specific CVDs such as diabetic cardiomyopathy (DCM), atherosclerosis (AS), and myocardial infarction (MI). In this paper, we collected previous research on lncRNA-mediated pyroptosis and investigated its pathophysiological significance in several cardiovascular illnesses. Interestingly, certain cardiovascular disease models and therapeutic medications are also under the control of lncRNa-mediated pyroptosis regulation, which may aid in the identification of new diagnostic and therapy targets. The discovery of pyroptosis-related lncRNAs is critical for understanding the etiology of CVD and may lead to novel targets and strategies for prevention and therapy.

AGE RAGE Pathways: Cardiovascular Disease and Oxidative Stress.

It is well established that Advanced Glycation End Products (AGEs) and their receptor (RAGE) are primarily responsible for the development of cardiovascular disease. As a result, diabetic therapy is very interested in therapeutic strategies that can target the AGE-RAGE axis. The majority of the AGE-RAGE inhibitors showed encouraging outcomes in animal experiments, but more information is needed to completely understand their clinical effects. The main mechanism implicated in the aetiology of cardiovascular disease in people with diabetes is oxidative stress and inflammation mediated by AGE-RAGE interaction. Numerous PPAR-agonists have demonstrated favourable outcomes in the treatment of cardio-metabolic illness situations by inhibiting the AGE-RAGE axis. The body's ubiquitous phenomena of inflammation occur in reaction to environmental stressors such tissue damage, infection by pathogens, or exposure to toxic substances. Rubor (redness), calor (heat), tumour (swelling), colour (pain), and in severe cases, loss of function, are its cardinal symptoms. When exposed, the lungs develop silicotic granulomas with the synthesis of collagen and reticulin fibres. A natural flavonoid called chyrsin has been found to have PPAR-agonist activity as well as antioxidant and anti-inflammatory properties. The RPE insod2+/animals underwent mononuclear phagocyte-induced apoptosis, which was accompanied with decreased superoxide dismutase 2 (SOD2) and increased superoxide generation. Injections of the serine proteinase inhibitor SERPINA3K decreased proinflammatory factor expression in mice with oxygen-induced retinopathy, decreased ROS production, and increased levels of SOD and GSH.

Inflammatory microRNAs in cardiovascular pathology: another brick in the wall.

The regulatory role of microRNAs (miRNAs) is mainly mediated by their effect on protein expression and is recognized in a multitude of pathophysiological processes. In recent decades, accumulating evidence has interest in these factors as modulatory elements of cardiovascular pathophysiology. Furthermore, additional biological processes have been identified as new components of cardiovascular disease etiology. In particular, inflammation is now considered an important cardiovascular risk factor. Thus, in the present review, we will focus on the role of a subset of miRNAs called inflamma-miRs that may regulate inflammatory status in the development of cardiovascular pathology. According to published data, the most representative candidates that play functional roles in thromboinflammation are miR-21, miR-33, miR-34a, miR-146a, miR-155, and miR-223. We will describe the functions of these miRNAs in several cardiovascular pathologies in depth, with specific emphasis on the molecular mechanisms related to atherogenesis. We will also discuss the latest findings on the role of miRNAs as regulators of neutrophil extracellular traps and their impact on cardiovascular diseases. Overall, the data suggest that the use of miRNAs as therapeutic tools or biomarkers may improve the diagnosis or prognosis of adverse cardiovascular events in inflammatory diseases. Thus, targeting or increasing the levels of adequate inflamma-miRs at different stages of disease could help mitigate or avoid the development of cardiovascular morbidities.

Emerging Roles of Gut Microbial Modulation of Bile Acid Composition in the Etiology of Cardiovascular Diseases.

Despite advances in preventive measures and treatment options, cardiovascular disease (CVD) remains the number one cause of death globally. Recent research has challenged the traditional risk factor profile and highlights the potential contribution of non-traditional factors in CVD, such as the gut microbiota and its metabolites. Disturbances in the gut microbiota have been repeatedly associated with CVD, including atherosclerosis and hypertension. Mechanistic studies support a causal role of microbiota-derived metabolites in disease development, such as short-chain fatty acids, trimethylamine-N-oxide, and bile acids, with the latter being elaborately discussed in this review. Bile acids represent a class of cholesterol derivatives that is essential for intestinal absorption of lipids and fat-soluble vitamins, plays an important role in cholesterol turnover and, as more recently discovered, acts as a group of signaling molecules that exerts hormonal functions throughout the body. Studies have shown mediating roles of bile acids in the control of lipid metabolism, immunity, and heart function. Consequently, a picture has emerged of bile acids acting as integrators and modulators of cardiometabolic pathways, highlighting their potential as therapeutic targets in CVD. In this review, we provide an overview of alterations in the gut microbiota and bile acid metabolism found in CVD patients, describe the molecular mechanisms through which bile acids may modulate CVD risk, and discuss potential bile-acid-based treatment strategies in relation to CVD.