Search Results (166)

Atherosclerosis is a progressive, multifactorial disease driven by the interplay of lipid dysregulation, chronic inflammation, oxidative stress, and maladaptive vascular remodeling. Despite advances in systemic lipid-lowering and anti-inflammatory therapies, residual cardiovascular risk persists, highlighting the need for more precise interventions. Targeted drug delivery represents a transformative strategy, offering the potential to modulate key pathogenic processes within atherosclerotic plaques while minimizing systemic exposure and off-target effects. Recent innovations span a diverse array of platforms, including nanoparticles, liposomes, exosomes, polymeric carriers, and metal–organic frameworks (MOFs), engineered to engage distinct pathological features such as inflamed endothelium, dysfunctional macrophages, oxidative microenvironments, and aberrant lipid metabolism. Ligand-based, biomimetic, and stimuli-responsive delivery systems further enhance spatial and temporal precision. In parallel, advances in in-silico modeling and imaging-guided approaches are accelerating the rational design of multifunctional nanotherapeutics with theranostic capabilities. Beyond targeting lipids and inflammation, emerging strategies seek to modulate immune checkpoints, restore endothelial homeostasis, and reprogram plaque-resident macrophages. This review provides an integrated overview of the mechanistic underpinnings of atherogenesis and highlights state-of-the-art targeted delivery systems under preclinical and clinical investigation. By synthesizing recent advances, we aim to elucidate how precision-guided drug delivery is reshaping the therapeutic landscape of atherosclerosis and to chart future directions toward clinical translation and personalized vascular medicine. Full article

The cement industry, a foundation of global infrastructure development, significantly contributes to environmental pollution. Key sources of pollution include dust emissions; greenhouse gases, particularly carbon dioxide; and the release of toxic substances such as heavy metals and particulate matter. These pollutants contribute to air, water, and soil degradation and are linked to severe health conditions in nearby populations, including respiratory disorders, cardiovascular diseases, and increased mortality rates. Noise pollution is also a significant issue, inducing auditory diseases that affect most workers in cement plants, and disturbing the population living in the neighborhoods and fauna behavior. This review explores the pollution paths and the multifaceted impacts of cement production on the environment. It also highlights the social challenges faced by communities, underscoring the urgent need for stricter environmental policies and the adoption of greener technologies to mitigate the adverse effects of cement production on both the environment and human health. Full article

Melatonin (MEL)is an endogenous hormone with antioxidant potential that plays an important role in maintaining redox homeostasis. MEL and its derivatives directly scavenge free oxygen and nitrogen radicals. Melatonin inhibits lipid peroxidation, stimulates antioxidant enzymes, and reduces metal toxicity. It stabilizes mitochondrial activity and suppresses inflammatory signaling. It takes part in neurogenesis, neuroprotection, and modulation of the cardiovascular system. It prevents many diseases of free radical etiology, i.e., neurodegenerative and circulatory system diseases and ischemic stroke. Supplementation with this antioxidant can slow down the aging process and provide protection against diseases of the central nervous system and support the body’s natural antioxidant system. This study uses current reports from the literature and meta-analyses of the antioxidant mechanisms of melatonin and its importance in neurodegenerative diseases. Full article

Cardiovascular diseases (CVDs) remain a leading cause of death globally and in Colombia. Oxidative stress plays a key role in CVD pathogenesis by promoting endothelial damage. Antioxidant compounds from fruits can mitigate oxidative stress through free radical scavenging and metal ion chelation. This review highlights tropical fruits rich in phenolic compounds and evaluates their antioxidant capacity using FRAP and DPPH methods. Evidence supports the inverse relationship between antioxidant intake and CVD incidence. Given Colombia’s fruit diversity, assessing dietary antioxidant capacity may inform strategies to improve diet quality and reduce CVD risk in the population. Full article

Heavy metal contamination, particularly lead (Pb) poisoning, is a significant public health issue worldwide. In Bangladesh, Pb contamination of water, soil, air, and food is detected alarmingly. Chronic exposure to Pb leads to severe health complications in the human body, including neurotoxicity, cardiovascular disease, developmental delays, and kidney damage. Research has established that there is “no safe level” of Pb exposure, as even minimal exposure can cause detrimental effects. Although existing physical and chemical methods are widely used, they come with limitations, such as high costs and the generation of toxic byproducts. As a green, sustainable alternative, the potential of probiotics as an effective biosorption agent has been explored to reduce Pb contamination in food, especially meat, while preserving its nutritional and sensory properties. This paper aims to integrate current knowledge from these two fields and highlight their capacity to decontaminate Pb-laden meat, the primary protein source in Bangladesh. The study also investigates optimal biosorption parameters, including temperature, pH, and exposure time, to enhance effectiveness. The proposed application of lactic acid bacteria (LAB) in meat processing and packaging is expected to significantly lower Pb levels in meat, ensuring safer consumption. Full article

Environmental exposure to heavy metals seriously threatens children’s health, potentially impacting the cardiovascular system. Mechanisms such as oxidative stress, inflammation, and lipid metabolism disturbances play a significant role in this process. Although cardiovascular diseases typically manifest in adulthood, an increasing number of studies suggest that their origins trace back to childhood and result from long-term pathophysiological changes. Therefore, early identification of modifiable risk factors is crucial for effective preventive measures and reducing future health risks. Full article

Environmental exposures to heavy metals, polychlorinated biphenyls (PCBs), dioxins, and furans have been associated with adverse cardiovascular outcomes, yet their combined effects remain underexplored. This study examined the joint influence of these contaminants on cardiovascular risk indicators in a representative sample of U.S. adults from the 2003–2004 National Health and Nutrition Examination Survey (NHANES). Biomarkers of exposure included lead, cadmium, mercury, twelve PCB congeners, seven dioxins, and ten furans. Cardiovascular outcomes were assessed using blood pressure, Framingham Risk Score (FRS), and lipid profiles. Associations were analyzed using multivariable linear regression and Bayesian Kernel Machine Regression (BKMR), adjusting for age, sex, ethnicity, body mass index, smoking, alcohol consumption, and income. The results demonstrated that metals, particularly mercury, were strongly associated with increased blood pressure and altered HDL cholesterol. PCBs were predominantly linked to elevated systolic blood pressure and FRS, with PCB156 and PCB126 identified as principal contributors. Furans exhibited the strongest associations with dyslipidemia, including elevated LDL cholesterol, total cholesterol, and triglycerides. Combined exposure analysis revealed a complex pattern, with increasing pollutant burdens associated with rising blood pressure and risk scores but declining lipid levels. These findings underscore the outcome-specific effects of pollutant mixtures and suggest that chronic low-level exposure to multiple environmental contaminants may contribute to cardiovascular dysfunction in the general population. Further longitudinal research is needed to confirm these associations and guide risk reduction strategies. Full article

The rapid development of nanotechnology has led to increased human exposure to metal-based nanoparticles (MNPs) through inhalation, ingestion, and dermal contact, raising growing concerns on their potential health effects. Due to their nanoscale size and unique physicochemical properties, the MNPs can translocate from the initial exposure sites to the circulatory system and accumulate in the body. This review focuses on MNP-induced cardiovascular toxicity, highlighting its biodistribution, cytotoxic mechanisms, and pathological impact associated with various cardiovascular diseases. MNPs disrupt endothelial function, promote oxidative stress, and induce apoptosis and ferroptosis in cardiovascular cells. Furthermore, MNPs increase endothelial permeability, impair blood–brain barrier integrity, and enhance procoagulant activity, thereby contributing to vascular and cardiac dysfunction. The particles and their released metal ions play a synergistic role in mediating these toxic effects. Here, we focused on the effects of nano-sized particles while incorporating recent in vitro and in vivo studies that address the cardiovascular impacts and mechanisms of MNP-induced toxicity. This comprehensive review will help understand and explain the potentially toxic effects of MNPs on the cardiovascular system. Full article

This study assessed the relationship between environmental chemical mixtures—including metals, per- and polyfluoroalkyl substances (PFAS), phthalates, and plasticizers—and key cardiovascular health markers using data from the 2013–2014 National Health and Nutrition Examination Survey (NHANES). The combined effects of these pollutants on cardiovascular markers were evaluated using Bayesian Kernel Machine Regression (BKMR), a flexible, non-parametric modeling approach that accommodates nonlinear and interactive relationships among exposures. BKMR was applied to assess both the joint and individual associations of the chemical mixture with systolic blood pressure (SBP), high-density lipoprotein (HDL), low-density lipoprotein (LDL), diastolic blood pressure (DBP), total cholesterol, and triglycerides. As part of the BKMR analysis, posterior inclusion probabilities (PIPs) were estimated to identify the relative importance of each exposure within the mixture. These results highlighted phthalates as major contributors to LDL, SBP, total cholesterol, HDL, and triglycerides while plasticizers were associated with LDL, SBP, HDL, and triglycerides. Metals and PFAS were most strongly linked to LDL, DBP, total cholesterol, and SBP. The overall mixture effect indicated that cumulative exposures were associated with lower LDL and SBP and elevated DBP, suggesting an increased cardiovascular risk. Triglycerides exhibited a complex quantile-dependent trend, with higher exposures associated with reduced levels. These findings underscore the importance of mixture-based risk assessments that reflect real-world exposure scenarios. Full article

Background: Cardiovascular disease (CVD) is a major global health burden influenced by genetic, behavioral, and environmental factors. Among these, exposure to per- and poly-fluoroalkyl substances (PFASs) and toxic metals has been increasingly implicated in adverse cardiovascular outcomes. However, the mediating role of dietary inflammation in these associations remains unclear. Objective: This study investigates the relationship between PFAS and metal exposures and CVD risk, focusing on the potential mediating role of diet, operationalized through the Dietary Inflammatory Index (DII). Additionally, this study examines age as an effect modifier in these associations. Methods: Utilizing data from the National Health and Nutrition Examination Survey (NHANES) 2017–2018 cycle (n = 660), we assessed environmental exposures (lead, cadmium, mercury, perfluorooctanoic acid-PFOA, perfluorooctane sulfonate-PFOS), dietary inflammatory potential (DII), and cardiovascular markers (blood pressure, lipid profile, C-reactive protein). Statistical analyses included linear regression and Bayesian Kernel Machine Regression-Causal Mediation Analysis (BKMR-CMA) to estimate the direct, indirect (through DII), and total effects of exposure on CVD risk biomarkers. Results: Linear regression revealed significant associations between mercury and reduced systolic blood pressure (SBP) (p = 0.017) and cadmium with increased C-reactive protein (CRP) (p = 0.006). Mediation analysis suggested dietary inflammation may play a role, though estimates were imprecise. Conclusions: PFAS and metals may influence CVD risk through inflammatory pathways, with potential age-related differences. Future longitudinal studies are needed to clarify these complex interactions, reduce measurement error, and guide age-specific exposure regulations. Full article

Cardiovascular diseases (CVDs) remain a leading global health concern, responsible for substantial morbidity and mortality. In recent years, as our understanding of the multifaceted nature of CVDs has increased, it has become increasingly evident that traditional risk factors alone do not account for the entirety of cardiovascular morbidity and mortality. Environmental toxins, a heterogeneous group of substances ubiquitous in our surroundings, have now entered the spotlight as offenders in the development and progression of CVDs. Environmental toxins include heavy metals, air pollutants, pesticides, and endocrine-disrupting chemicals, among others. Upon exposure, they can elicit oxidative stress, a condition characterized by an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify and repair the resulting damage. Oxidative stress triggers a cascade of events, including inflammation, endothelial dysfunction, lipid peroxidation, and vascular remodeling, which can contribute to the development of atherosclerosis, hypertension, and other cardiovascular pathologies. This article delves into the molecular mechanisms underpinning oxidative stress-mediated cardiovascular damage induced by environmental toxins, emphasizing the role of specific toxins in this process. Further research is necessary to understand how individual susceptibility and genotype influence the impact of environmental toxins on oxidative stress and the risk of CVD. Full article

Cardiovascular diseases (CVDs) are the leading cause of mortality globally, accounting for approximately one-third of all deaths. Exposure to toxic metals poses significant risks to cardiovascular health, contributing to the development of CVDs. Essential elements are crucial for maintaining cardiovascular function; however, imbalances or deficiencies in these elements can exacerbate the risk and progression of CVDs. Understanding the interactions between toxic metals and essential elements is crucial for elucidating their impact on cardiovascular health. This study aims to examine the individual and combined effects of toxic metals—lead (Pb), cadmium (Cd), and mercury (Hg)—along with essential elements—manganese (Mn), iron (Fe), and selenium (Se)—on CVDs. We explored the effects of toxic metals and essential elements using data from the National Health and Nutrition Examination Survey (NHANES, 2017–2018). We conducted descriptive analyses and applied advanced statistical methods, including Bayesian kernel machine regression (BKMR), weighted quantile sum regression (WQSR), and quantile g-computation, to assess the associations between these toxic metals and essential elements on key cardiovascular-related biomarkers. The results revealed distinct patterns of influence across the toxic metals and essential elements. Spearman correlation showed a stronger association among toxic metals than essential elements. Bayesian kernel machine regression (BKMR) and posterior inclusion probability (PIP) analysis identified lead, mercury, iron, and selenium as key contributors to CVD risk, with lead strongly linked to high-density lipoprotein (HDL), diastolic blood pressure (DBP), and systolic blood pressure (SBP). Selenium was linked to low-density lipoprotein (LDL) cholesterol and non-high-density lipoprotein (non-HDL) cholesterol. Univariate and bivariate analyses confirmed lead and mercury’s strong associations with triglycerides and blood pressure, while lead, selenium, and iron were linked to different cholesterol outcomes. Single-variable analysis revealed an interaction between individual exposures and combined exposures. The overall exposure effect assessing the impact of all exposures combined on CVD markers revealed a steady positive association with triglycerides, total cholesterol, LDL, non-HDL cholesterol, and DBP, with HDL and SBP increasing from the 65th percentile. Quantile g-computation and WQSR confirmed lead’s consistent positive association across all outcomes, with variations among other toxic metals and essential elements. In conclusion, our study suggests that toxic metals and essential elements are important factors in CVD outcomes, with different metals and elements associated with variations in specific biomarkers. Full article

Alpha-lipoic acid (ALA) is an essential organosulfur compound with a wide range of therapeutic applications, particularly in conditions involving inflammation and oxidative stress. In this review, we describe our current understanding of the multifaceted role of ALA in several inflammatory diseases (acute pancreatitis, arthritis, osteoarthritis, asthma, and sepsis), cardiovascular disorders (CVDs), and neurological conditions. The dual redox nature of ALA, shared with its reduced form dihydrolipoic acid (DHLA), underpins its powerful antioxidant and anti-inflammatory properties, including reactive oxygen species scavenging, metal chelation, and the regeneration of endogenous antioxidants such as glutathione. A substantial body of evidence from preclinical and clinical studies suggests that ALA modulates the key signaling pathways involved in inflammation and cellular stress responses, making it a promising candidate for mitigating inflammation and its systemic consequences. Notably, we also discuss a novel perspective that attributes some of the therapeutic effects of ALA to its ability to release hydrogen sulfide (H₂S), a gaseous signaling molecule. This mechanism may offer further insights into the efficacy of ALA in the treatment of several diseases. Together, these findings support the potential of ALA as a multifunctional agent for managing inflammatory and oxidative stress-related diseases. Full article

α-Lipoic acid (ALA) is a naturally occurring compound with diverse biological functions, widely distributed in animal and plant tissues. It has attracted considerable attention due to its versatile therapeutic potential. However, despite these promising prospects, the clinical application of ALA remains limited by its low bioavailability and chemical instability and an incomplete understanding of its multifaceted mechanisms across various diseases. This review provides a comprehensive overview of the biochemical properties of ALA, including its direct free-radical-scavenging activity, regeneration of endogenous antioxidants, chelation of metal ions, and modulation of inflammatory responses. We also highlight the current evidence regarding ALA’s therapeutic roles and efficacy in major diseases, such as neurodegenerative disorders, lung diseases, cardiovascular diseases, and diabetes. Furthermore, recent advancements and innovative strategies in ALA-based derivatives and drug-delivery systems are summarized, emphasizing their potential to address complex diseases and the necessity for further translational studies. This review aims to provide a theoretical foundation for the rational design of ALA-based therapies, thereby supporting future clinical applications and the optimization of therapeutic strategies. Full article

Background/Objectives: Cardiovascular diseases (CVDs) are the leading cause of global mortality. Major adverse cardiovascular events (MACEs)—such as acute myocardial infarction, stroke, and heart failure—are critical endpoints in the clinical research. The existing research has shown metal ions are important regulators of cardiovascular functioning, and defective metal handling may be associated with an increased risk of CVD. This study examines the association of the plasma/serum levels of magnesium, copper, and zinc with MACE incidence and the prevalence of circulatory system diseases, by using electronic health records from a subset of the Scottish population. Methods: We categorised individuals by high, low, or normal plasma/serum metal levels, and calculated the percentage of those who subsequently developed a MACE, identified using related International Classification of Diseases, 10th Revision codes from hospital admission records. Logistic regression was employed to analyse the association between pre-event metal ion levels and the development of specific circulatory system disease subgroups. Results: This study found abnormal magnesium, high copper, and low zinc were associated with a higher risk of developing MACEs. Low magnesium, high copper, or low zinc were associated with increased risks of various circulatory diseases, with specific variations, like low copper increasing venous and lymphatic disease risk. Conclusions: Our findings suggest abnormal plasma metal profiles are associated with the development of MACEs and circulatory disease events, underscoring the importance of monitoring plasma metal levels for cardiovascular risk management and prevention. Full article