Inflammatory Cardiovascular Diseases Research Articles

Reinventing gut health: leveraging dietary bioactive compounds for the prevention and treatment of diseases.

The human gut harbors a complex and diverse microbiota essential for maintaining health. Diet is the most significant modifiable factor influencing gut microbiota composition and function, particularly through bioactive compounds like polyphenols, dietary fibers, and carotenoids found in vegetables, fruits, seafood, coffee, and green tea. These compounds regulate the gut microbiota by promoting beneficial bacteria and suppressing harmful ones, leading to the production of key microbiota-derived metabolites such as short-chain fatty acids, bile acid derivatives, and tryptophan metabolites. These metabolites are crucial for gut homeostasis, influencing gut barrier function, immune responses, energy metabolism, anti-inflammatory processes, lipid digestion, and modulation of gut inflammation. This review outlines the regulatory impact of typical bioactive compounds on the gut microbiota and explores the connection between specific microbiota-derived metabolites and overall health. We discuss how dietary interventions can affect disease development and progression through mechanisms involving these metabolites. We examine the roles of bioactive compounds and their metabolites in the prevention and treatment of diseases including inflammatory bowel disease, colorectal cancer, cardiovascular diseases, obesity, and type 2 diabetes mellitus. This study provides new insights into disease prevention and underscores the potential of dietary modulation of the gut microbiota as a strategy for improving health.

The effect of macrophage-cardiomyocyte interactions on cardiovascular diseases and development of potential drugs.

The interaction between macrophages and cardiomyocytes plays an important role not only in maintaining cardiac homeostasis, but also in the development of many cardiovascular diseases (CVDs), such as myocardial infarction (MI) and heart failure (HF). In addition to supporting cardiomyocytes, macrophages and cardiomyocytes have a close and complex relationship. By studying their cross-talk, we can better understand novel mechanisms and target pathogenic mechanisms, and improve the treatment of CVDs. We review macrophage-cardiomyocyte communication through connexin 43 (Cx43)-containing gap junctions (GJs) directly, secreted protein factors indirectly, and discuss the implications of these interactions in cardiac homeostasis and the development of various CVDs, including MI, HF, arrhythmia, cardiac fibrosis and myocarditis. In this section, we review various drugs that work by modulating cytokines or other proteins to reduce inflammation in CVDs. The clinical findings from targeting inflammation in CVDs are also discussed. Additionally, we examine the challenges and opportunities for improving our understanding of macrophage-cardiomyocyte coupling as it relates to pathophysiological disease processes, extending our research scope, and helping identify new molecular targets and improve the effectiveness of existing therapies.

Blue Mussel-Derived Bioactive Peptides PIISVYWK (P1) and FSVVPSPK (P2): Promising Agents for Inhibiting Foam Cell Formation and Inflammation in Cardiovascular Diseases.

Atherosclerosis is a key etiological event in the development of cardiovascular diseases (CVDs), strongly linked to the formation of foam cells. This study explored the effects of two blue mussel-derived bioactive peptides (BAPs), PIISVYWK (P1) and FSVVPSPK (P2), on inhibiting foam cell formation and mitigating inflammation in oxLDL-treated RAW264.7 macrophages. Both peptides significantly suppressed intracellular lipid accumulation and cholesterol levels while promoting cholesterol efflux by downregulating cluster of differentiation 36 (CD36) and class A1 scavenger receptors (SR-A1) and upregulating ATP binding cassette subfamily A member 1 (ABCA-1) and ATP binding cassette subfamily G member 1 (ABCG-1) expressions. The increased expression of peroxisome proliferator-activated receptor-gamma (PPAR-γ) and liver X receptor-alpha (LXR-α) further validated their role in enhancing cholesterol efflux. Additionally, P1 and P2 inhibited foam cell formation in oxLDL-treated human aortic smooth muscle cells and exerted anti-inflammatory effects by reducing pro-inflammatory cytokines, nitric oxide (NO), prostaglandin E2 (PGE2), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), primarily through inhibiting NF-κB activation. Furthermore, P1 and P2 alleviated oxidative stress by activating the Nrf2/HO-1 pathway. Our findings demonstrate that P1 and P2 have significant potential in reducing foam cell formation and inflammation, both critical factors in atherosclerosis development. These peptides may serve as promising therapeutic agents for the prevention and treatment of CVDs associated with oxidative stress and inflammation.

Novel Therapeutics and Upcoming Clinical Trials Targeting Inflammation in Cardiovascular Diseases.

Cardiovascular disease (CVD) remains a major health burden despite significant therapeutic advances accomplished over the last decades. It is widely and increasingly recognized that systemic inflammation not only represents a major cardiovascular risk and prognostic factor but also plays pivotal roles in CVD development and progression. Despite compelling preclinical evidence suggesting large potential of anti-inflammatory pharmacological interventions across numerous CVDs, clinical translation remains incomplete, mainly due to (1) yet undefined molecular signaling; (2) challenges of safety and efficacy profile of anti-inflammatory drugs; and (3) difficulties in identifying optimal patient candidates and responders to anti-inflammatory therapeutics, as well as optimal therapeutic windows. Randomized controlled trials demonstrated the safety/efficacy of canakinumab and colchicine in secondary cardiovascular prevention, providing confirmation for the involvement of a specific inflammatory pathway (NLRP3 [NACHT, LRR, and PYD domain-containing protein 3] inflammasome/IL [interleukin]-1β) in atherosclerotic CVD. Colchicine was recently approved by the US Food and Drug Administration for this indication. Diverse anti-inflammatory drugs targeting distinct inflammatory pathways are widely used for the management of other CVDs including myocarditis and pericarditis. Ongoing research efforts are directed to implementing anti-inflammatory therapeutics across a growing number of CVDs, through repurposing of available anti-inflammatory drugs and development of novel anti-inflammatory compounds, which are herein concisely discussed. This review also summarizes the main characteristics and findings of completed and upcoming randomized controlled trials directly targeting inflammation in CVDs and discusses the major challenges and future perspectives in the exciting and constantly expanding landscape of cardioimmunology.

Involvement of pentraxin-3 in the development of hypertension but not left ventricular hypertrophy in male spontaneously hypertensive rats.

Hypertension drives the development of concentric left ventricular hypertrophy (LVH). However, the relative contribution of pentraxin-3 (PTX-3), a novel marker for inflammatory cardiovascular disease, in the hypertrophic response to pressure overload has not been adequately elucidated. We investigated the role of PTX-3 in the development of LVH in spontaneously hypertensive rats (SHR), untreated and treated with either captopril (an ACE inhibitor) or hydralazine (a non-specific vasodilator). Three-month-old SHR received either 20 mg/kg/day hydralazine (SHR + H, n = 6), 40 mg/kg/day captopril (SHR + C, n = 6), or plain gelatine cubes (untreated SHR, n = 7) orally for 4 months. Wistar Kyoto rats (WKY, n = 7) were used as the normotensive controls. Blood pressure (BP) was measured using the tail-cuff method. Cardiac geometry and function were determined using M-mode echocardiography. Circulating concentrations of inflammatory markers were measured in plasma by ELISA. LV fibrosis and cardiomyocyte width were assessed by histology. Relative mRNA expression of PTX-3 was determined in the LV by RT-PCR. Untreated SHR exhibited greater systolic BP and relative wall thickness (RWT) compared to WKY. Captopril and hydralazine normalized BP but only captopril reversed RWT in SHR. Circulating PTX-3 and VCAM-1 levels were elevated in untreated SHR and reduced with captopril and hydralazine. Circulating PTX-3 was positively associated with systolic BP but lacked independent relations with indices of LVH. LV relative mRNA expression of PTX-3 was similar between the groups. PTX-3 may not be involved in the development of LVH in SHR, but plausibly reflects the localized inflammatory milieu associated with hypertension.

The role of biomarkers on hemodynamics in atherosclerotic artery

Atherosclerosis, a chronic inflammatory cardiovascular disease, leads to arterial constriction caused by the accumulation of lipids, cholesterol, and various substances within artery walls. Such plaque can rupture, resulting in a blood clot that obstructs major arteries and may initiate myocardial infarction, ischemic stroke, etc. Atherosclerotic plaque formation begins with the accumulation of foam cells and macrophages within the intima layer of the arterial wall. At the latter stage, the smooth muscle cells migrated from deeper artery wall layers, contributing to the fibrous cap formation and plaque stabilizing. A developed plaque gradually enters the lumen and narrows down the lumen to impede blood flow. We introduce a two-phase and macroscopic model to investigate the progression of plaque growth in its advanced stage and analyze the minimum gap (Lumen Clearance) within an atherosclerotic artery so that blood cells can pass through. Cardiac troponin, a high specificity and sensitivity biomarker, facilitates early detection of elevated myocardial infarction, ischemic stroke risks, etc. This study aims at establishing a relationship between the troponin concentration in atherosclerotic arteries and their internal clearance, which could significantly improve our understanding of disease progression. Our observations show that the plaque undergoes rapid evolution in its initial stages, gradually slowing down over time to reach a stable state. A positive correlation exists between the maximum plaque depth and cardiac troponin concentration in the blood. However, the lumen clearance exhibits the opposite behavior. The speed of blood cells slows down at an enhanced plaque depth within atherosclerotic arteries.

The human milk oligosaccharide 3'sialyllactose reduces low-grade inflammation and atherosclerosis development in mice.

Macrophages contribute to the induction and resolution of inflammation and play a central role in chronic low-grade inflammation in cardiovascular diseases caused by atherosclerosis. Human milk oligosaccharides (HMOs) are complex unconjugated glycans unique to human milk that benefit infant health and act as innate immune modulators. Here, we identify the HMO 3'sialyllactose (3'SL) as a natural inhibitor of Toll-Like Receptor (TLR) 4-induced low-grade inflammation in macrophages and endothelium. Transcriptome analysis in macrophages revealed that 3'SL attenuates mRNA levels of a selected set of inflammatory genes and promotes the activity of Liver X Receptor (LXR) and Sterol Regulatory Element-binding Protein-1 (SREBP). These acute anti-inflammatory effects of 3'SL were associated with reduced histone H3K27 acetylation at a subset of lipopolysaccharide (LPS)-inducible enhancers distinguished by preferential enrichment for CCCTC-binding factor (CTCF), Interferon Regulatory Factor 2 (IRF2), B-cell lymphoma 6 (BCL6), and other transcription factor recognition motifs. In a murine atherosclerosis model, both subcutaneous and oral administration of 3'SL significantly reduced atherosclerosis development and the associated inflammation. This study provides evidence that 3'SL attenuates inflammation by a transcriptional mechanism to reduce atherosclerosis development in the context of cardiovascular disease.

Role of lymphocyte-to-monocyte ratio as a predictive marker for diabetic coronary artery disease: A cross-sectional study.

The lymphocyte to monocyte ratio (LMR) is considered a marker of systemic inflammation in cardiovascular disease and acts as predictor of mortality in coronary artery disease. To investigate the predictive role of LMR in diabetic coronary artery disease patients. This cross-sectional study was conducted at tertiary care super-specialty hospital at New Delhi, India. A total of 200 angiography-proven coronary artery disease (CAD) patients were enrolled and grouped into two categories: Group I [CAD patients with type 2 diabetes mellitus (T2DM) and glycated hemoglobin (HbA1c) levels ≥ 6.5%], and Group II (CAD patients without T2DM and HbA1c levels < 6.5%). Serum lipoproteins, HbA1c, and complete blood count of enrolled patients were analyzed using fully automatic analyzers. The logistic regression analysis showed an odds ratio of 1.48 (95%CI: 1.28-1.72, P < 0.05) for diabetic coronary artery disease patients (Group I) in unadjusted model. After adjusting for age, gender, diet, smoking, and hypertension history, the odds ratio increased to 1.49 (95%CI: 1.29-1.74, P < 0.01) in close association with LMR. Further adjustment for high cholesterol and triglycerides yielded the same odds ratio of 1.49 (95%CI: 1.27-1.75, P < 0.01). Receiver operating characteristic curve analysis revealed 74% sensitivity, 64% specificity, and 0.74 area under the curve (95%CI: 0.67-0.80, P < 0.001), suggesting moderate predictive accuracy for diabetic CAD patients. LMR showed positive association with diabetic coronary artery disease, with moderate predictive accuracy. These findings have implications for improving CAD management in diabetics, necessitating further research and targeted interventions.

Bioelectronic Medicines-A Novel Approach of Therapeutics in Current Epoch.

Bioelectronic medicines aim to diagnose and treat a wide range of illnesses and ailments, including cancer, rheumatoid arthritis, inflammatory bowel disease, obesity, diabetes, asthma, paralysis, blindness, bleeding, ischemia, organ transplantation, cardiovascular disease, and neurodegenerative diseases. The focus of bioelectronic medicine is on electrical signaling of the nervous system. Understanding the nervous system's regulatory roles and developing technologies that record, activate, or inhibit neural signaling to influence particular biological pathways. Bioelectronic medicine is an emerging therapeutic option with the interconnection between molecular medicine, neuroscience, and bioengineering. The creation of nerve stimulating devices that communicate with both the central and peripheral nervous systems has the potential to completely transform how we treat disorders. Although early clinical applications have been largely effective across entire nerves, the ultimate goal is to create implantable, miniature closed-loop systems that can precisely identify and modulate individual nerve fibers to treat a wide range of disorders. The data bases such as PubMed, and Clinicaltrial.gov.in were searched for scientific research, review and clinical trials on bioelectronic medicine. The field of bioelectronic medicine is trending at present. In recent years, researchers have extended the field's applications, undertaken promising clinical trials, and begun delivering therapies to patients, thus creating the groundwork for significant future advancements. Countries and organizations must collaborate across industries and regions to establish an atmosphere and guidelines that foster the advancement of the field and the fulfillment of its prospective advantages.

Deciphering the Causal Links: A Mendelian Randomization Study of Circulating Inflammatory Proteins and Cardiovascular Diseases

Objective: The main objective was to gain a deeper understanding of the underlying mechanisms of cardiovascular illnesses and to identify the key components and potential treatment targets using Mendelian randomization (MR). Methods: This study utilizes a two-sample MR approach to examine the causal association between 91 circulating inflammatory proteins and four primary categories of cardiovascular disease. Results: Ultimately This study identifies 28 significant causal links with key findings revealing the correlation between Macrophage colony-stimulating factor 1 and both coronary artery disease and heart failure.Additionally, the study highlights the diverse functions of various interleukins in different cardiovascular diseases. Conclusions: Our analysis extends existing knowledge by uncovering potential therapeutic targets for peripheral artery disease, heart failure, and stroke, previously under-researched in the context of these inflammatory proteins. This research highlights the importance of inflammatory biomarkers in predicting cardiovascular events and opens new avenues for therapeutic intervention.

Oxidative Stress and Age-Related Tumors.

Oxidative stress is the result of the imbalance between reactive oxygen and nitrogen species (RONS), which are produced by several endogenous and exogenous processes, and antioxidant defenses consisting of exogenous and endogenous molecules that protect biological systems from free radical toxicity. Oxidative stress is a major factor in the aging process, contributing to the accumulation of cellular damage over time. Oxidative damage to cellular biomolecules, leads to DNA alterations, lipid peroxidation, protein oxidation, and mitochondrial dysfunction resulting in cellular senescence, immune system and tissue dysfunctions, and increased susceptibility to age-related pathologies, such as inflammatory disorders, cardiovascular and neurodegenerative diseases, diabetes, and cancer. Oxidative stress-driven DNA damage and mutations, or methylation and histone modification, which alter gene expression, are key determinants of tumor initiation, angiogenesis, metastasis, and therapy resistance. Accumulation of genetic and epigenetic damage, to which oxidative stress contributes, eventually leads to unrestrained cell proliferation, the inhibition of cell differentiation, and the evasion of cell death, providing favorable conditions for tumorigenesis. Colorectal, breast, lung, prostate, and skin cancers are the most frequent aging-associated malignancies, and oxidative stress is implicated in their pathogenesis and biological behavior. Our aim is to shed light on the molecular and cellular mechanisms that link oxidative stress, aging, and cancers, highlighting the impact of both RONS and antioxidants, provided by diet and exercise, on cellular senescence, immunity, and development of an antitumor response. The dual role of ROS as physiological regulators of cell signaling responsible for cell damage and diseases, as well as its use for anti-tumor therapeutic purposes, will also be discussed. Managing oxidative stress is crucial for promoting healthy aging and reducing the risk of age-related tumors.

Hydrogen Sulfide: A Versatile Molecule and Therapeutic Target in Health and Diseases.

In recent years, research has unveiled the significant role of hydrogen sulfide (H2S) in many physiological and pathological processes. The role of endogenous H2S, H2S donors, and inhibitors has been the subject of studies that have aimed to investigate this intriguing molecule. The mechanisms by which H2S contributes to different diseases, including inflammatory conditions, cardiovascular disease, viral infections, and neurological disorders, are complex. Despite noteworthy progress, several questions remain unanswered. H2S donors and inhibitors have shown significant therapeutic potential for various diseases. This review summarizes our current understanding of H2S-based therapeutics in inflammatory conditions, cardiovascular diseases, viral infections, and neurological disorders.

In adult Americans, there is an association between IBI levels and the prevalence of CVD in adult Americans: evidence from NHANES 2005–2010

AimsWe aimed to assess the association between Inflammatory Burden Index (IBI) and cardiovascular disease (CVD) in adult Americans. MethodsThis cross-sectional investigation included people with comprehensive data on IBI and CVD from the National Health and Nutrition Examination Survey (NHANES) 2005–2010 database. C-reactive protein (CRP) × neutrophil/lymphocyte (NLR) count was used to calculate IBI. CVD included angina pectoris, stroke, congestive heart failure (CHF), and coronary heart disease (CHD). Subgroup analysis and weighted multivariate regression were utilized to analyze the independent association between CVD and IBI. ResultsA total of 15,325 adult Americans were involved. There were 9.57 % of subjects having CVD, which was increased with increasing IBI quartiles (Tertile 1: 4.64 %; Tertile 2: 7.71 %; Tertile 3: 10.63 %; Tertile 4: 15.29 %; p < 0.001). After full adjustment, multivariate logistic regression analysis demonstrated a positive correlation between IBI level and CVD prevalence (OR = 1.43; 95 % CI, 1.16–1.76, p < 0.001). Subgroup analyses and interaction tests showed that the association between IBI and the prevalence of CVD was not affected by sex, age, body mass index, race, hypertension, and diabetes mellitus. ConclusionsIn adult Americans, There is an association between IBI levels and the prevalence of CVD. More large-scale future research is required to assess the effect of IBI on CVD.

High-Salt Diet and Intestinal Microbiota: Influence on Cardiovascular Disease and Inflammatory Bowel Disease.

Salt, or sodium chloride, is an essential component of the human diet. Recent studies have demonstrated that dietary patterns characterized by a high intake of salt can influence the abundance and diversity of the gut microbiota, and may play a pivotal role in the etiology and exacerbation of certain diseases, including inflammatory bowel disease and cardiovascular disease. The objective of this review is to synthesize the effects of elevated salt consumption on the gut microbiota, including its influence on gut microbial metabolites and the gut immune system. Additionally, this review will investigate the potential implications of these effects for the development of cardiovascular disease and inflammatory bowel disease. The findings of this study offer novel insights and avenues for the management of two common conditions with significant clinical implications.

A Comprehensive Review of the Triangular Relationship among Diet-Gut Microbiota-Inflammation.

The human gastrointestinal tract hosts a complex and dynamic community of microorganisms known as the gut microbiota, which play a pivotal role in numerous physiological processes, including digestion, metabolism, and immune function. Recent research has highlighted the significant impact of diet on the gut microbiota composition and functionality, and the consequential effects on host health. Concurrently, there is growing evidence linking the gut microbiota to inflammation, a key factor in many chronic diseases such as inflammatory bowel disease (IBD), obesity, diabetes, and cardiovascular diseases (CVDs). This review explores how dietary components influence the gut microbiota composition, how these microbial changes affect inflammatory pathways, and the therapeutic implications of modulating this axis for chronic inflammatory disease prevention and management. Beneficial dietary patterns, such as the Mediterranean diet (MD) and plant-based diets, promote a diverse and balanced gut microbiota composition, supporting anti-inflammatory pathways. Conversely, the Western diet (WD), high in saturated fats and refined sugars, is associated with dysbiosis and increased inflammation. With all the links between the three variables considered, this review attempts to offer a thorough examination of the triangle formed by inflammation, the gut microbiota, and food.

The role of inflammatory response in the development of atherosclerosis, myocardial infarction, and remodeling

Inflammation is an intrinsic part of the body’s immune response, significantly influencing a myriad of physiological and pathological processes. There is now clinical and experimental evidence suggesting that inflammation accelerates atherosclerosis and its associated complications. The presence of macrophages, T and B cells inside the atherosclerotic plaque fueled this concept and steered subsequent research endeavors toward understanding the pathophysiology of atherosclerosis including plaque formation and destabilization leading to plaque rupture resulting in myocardial injury and remodeling. Understanding the mechanism behind atherosclerosis will aid in developing appropriate treatment interventions. Shifting research and drug development from a singular focus on cholesterol-lowering agents to include adjunctive anti-inflammatory therapies is crucial. Targeting a root cause, i.e., inflammation, will help decrease the incidence and progression of atherosclerosis and improve patient outcomes. In this review, we aim to discuss the current understanding of the intricate role of inflammation in the pathogenesis of atherosclerosis, myocardial infarction, and cardiac remodeling. This synthesis will encompass an exploration of the various inflammatory cells involved, the intricate network of chemokines orchestrating inflammatory responses, and the pathways that underpin these cardiovascular conditions. Furthermore, we will explore promising diagnostic and therapeutic strategies aimed at addressing inflammation in cardiovascular diseases. These include interventions such as colchicine, monoclonal antibodies, and nanoparticles designed to deliver and accumulate drugs at the molecular level within cells.

Microbiota during pregnancy and early life: role in maternal-neonatal outcomes based on human evidence.

Here, we explored the vast potential of microbiome-based interventions in preventing and managing non-communicable diseases including obesity, diabetes, allergies, celiac disease, inflammatory bowel diseases, malnutrition, and cardiovascular diseases across different life stages. We discuss the intricate relationship between microbiome and non-communicable diseases, emphasizing on the "window of opportunity" for microbe-host interactions during the first years after birth. Specific biotics and also live biotherapeutics including fecal microbiota transplantation emerge as pivotal tools for precision medicine, acknowledging the "one size doesn't' fit all" aspect. Challenges in implementation underscore the need for advanced technologies, scientific transparency, and public engagement. Future perspectives advocate for understanding maternal-neonatal microbiome, exploring the maternal exposome and delving into human milk's role in the establishment and restoration of the infant microbiome and its influence over health and disease. An integrated scientific approach, employing multi-omics and accounting for inter-individual variance in microbiome composition and function appears central to unleash the full potential of early-life microbiome interventions in revolutionizing healthcare.

Causal effects of inflammatory cytokines on cardiovascular diseases: Insights from genetic evidence

BackgroundThe causal relationship between inflammatory cytokines and cardiovascular diseases (CVDs) has not been fully elucidated. Exploring this relationship between circulating inflammatory cytokines and CVDs is crucial for early clinical diagnosis and effective treatment. Methods and ResultsThis study investigated the causal relationships between 41 inflammatory cytokines and six CVDs: heart failure (HF), myocardial infarction (MI), unstable angina pectoris (UAP), stable angina pectoris (SAP), valvular heart disease (VHD), and aortic aneurysm (AA), using the Mendelian Randomization (MR) method. The primary analysis employed the inverse-variance weighted (IVW) method within MR. Heterogeneity and pleiotropy were assessed through MR-Egger regression and the Q statistic. Strong evidence supported the effect of macrophage inflammatory protein-1β (MIP-1β) on MI (OR = 1.062, P < 0.001, FDR <0.001). Suggestive evidence showed that the Beta nerve growth factor increased the risk of MI (OR = 1.145, P = 0.025), but the stem cell factor (SCF) demonstrated a potential protective effect against MI (OR = 0.910, P = 0.04). SCF and hepatocyte growth factor (HGF) exhibited potential protective effects against SAP. No inflammatory cytokine was associated with UAP. Monocyte chemotactic protein-1 was linked to an increased risk of VHD (OR = 1.056, P = 0.049). Higher levels of interleukin-13 (IL-13), interferon gamma-induced protein 10 (IP-10), and growth-regulated oncogene-alpha were associated with increased susceptibility to HF. Elevated basic fibroblast growth factor (bFGF) levels exhibited protective effects against AA (OR = 0.751, P = 0.038). Reverse MR analyses revealed that AA significantly decreased circulating TNF-related apoptosis-inducing ligand (TRAIL) levels (OR = 0.907, P < 0.001, FDR = 0.01). MI significantly increased circulating IL-12-p70 levels (OR = 1.146, P < 0.001, FDR = 0.014). Suggestive evidence indicated the Causal effects of six CVDs on 17 circulating inflammatory cytokines. ConclusionsThis study clarified the causal relationships between specific inflammatory cytokines and six CVDs, providing novel insights and evidence into the genetic involvement of inflammatory cytokines in CVDs. These inflammatory cytokines may be potential biomarkers for early disease diagnosis and treatment evaluation.

Understanding Galectin-3's Role in Diastolic Dysfunction: A Contemporary Perspective.

Diastolic dysfunction, a prevalent condition characterized by impaired relaxation and filling of the left ventricle, significantly contributes to heart failure with preserved ejection fraction (HFpEF). Galectin-3, a β-galactoside-binding lectin, has garnered attention as a potential biomarker and mediator of fibrosis and inflammation in cardiovascular diseases. This comprehensive review investigates the impact of galectin-3 on diastolic dysfunction. We explore its molecular mechanisms, including its involvement in cellular signaling pathways and interaction with components of the extracellular matrix. Evidence from both animal models and clinical studies elucidates galectin-3's role in cardiac remodeling, inflammation, and fibrosis, shedding light on the underlying pathophysiology of diastolic dysfunction. Additionally, we examine the diagnostic and therapeutic implications of galectin-3 in diastolic dysfunction, emphasizing its potential as both a biomarker and a therapeutic target. This review underscores the significance of comprehending galectin-3's role in diastolic dysfunction and its promise in enhancing diagnosis and treatment approaches for HFpEF patients.

Graphene Quantum Dots Inhibit Lipid Peroxidation in Biological Membranes.

Excessive reactive oxygen species (ROS) in cellular environments leads to oxidative stress, which underlies numerous diseases, including inflammatory diseases, neurodegenerative diseases, cardiovascular diseases, and cancer. Oxidative stress can be particularly damaging to biological membranes such as those found in mitochondria, which are abundant with polyunsaturated fatty acids (PUFAs). Oxidation of these biological membranes results in concomitant disruption of membrane structure and function, which ultimately leads to cellular dysfunction. Graphene quantum dots (GQDs) have garnered significant interest as a therapeutic agent for numerous diseases that are linked to oxidative stress. Specifically, GQDs have demonstrated an ability to protect mitochondrial structure and function under oxidative stress conditions. However, the fundamental mechanisms by which GQDs interact with membranes in oxidative environments are poorly understood. Here, we used C11-BODIPY, a fluorescent lipid oxidation probe, to develop quantitative fluorescence assays that determine both the extent and rate of oxidation that occurs to PUFAs in biological membranes. Based on kinetics principles, we have developed a generalizable model that can be used to assess the potency of antioxidants that scavenge ROS in the presence of biological membranes. By augmenting our fluorescence assays with 1H NMR spectroscopy, the results demonstrate that GQDs scavenge nascent hydroxyl and peroxyl ROS that interact with membranes and that GQDs are potent inhibitors of ROS-induced lipid oxidation in PUFA-containing biological membranes. The antioxidant potency of GQDs is comparable to or even greater than established antioxidant molecules, such as ascorbic acid and Trolox. This work provides mechanistic insights into the mitoprotective properties of GQDs under oxidative stress conditions, as well as a quantitative framework for assessing antioxidant interactions in biological membrane systems.