Chlorogenic acid (CGA), an ester of caffeic and quinic acids, is a dietary polyphenol abundant in coffee, tea, fruits, vegetables, and medicinal plants, with 5-O-caffeoylquinic acid (5-CQA) as its predominant isomer. This review aims to summarize current knowledge on the biological activities, mechanisms of action, and potential therapeutic applications of CGA in the prevention and management of metabolic disorders. CGA demonstrates a broad spectrum of biological activities relevant to human health. Its mechanisms of action involve modulation of oxidative stress and key cellular signaling pathways, as well as regulation of metabolic processes, contributing to improved insulin sensitivity, lipid balance, and overall energy homeostasis. These properties make CGA a promising agent against metabolic syndrome (type 2 diabetes, obesity, hypertension, and dyslipidemia) which is a major global health challenge. Despite its health benefits, CGA’s oral bioavailability remains limited, prompting research into optimized extraction methods, novel formulations, and structural modifications. Current evidence supports its safety even at high doses, reinforcing its potential as a nutraceutical, functional food ingredient, and adjunctive therapeutic compound in chronic disease management.

Cardiovascular diseases (CVDs) are increasingly being defined not only in terms of metabolic or purely vascular disorders, but also as complex immunometabolic disorders. One of the most groundbreaking discoveries in recent years is the role of neutrophil extracellular networks (NETs/NENs) as a key link between chronic vascular wall inflammation and thrombotic processes. In this article, we present a synthetic overview of the latest data on the biology of NETs/NENs and their impact on the development of atherosclerosis, endothelial dysfunction, and the mechanisms of immunothrombosis. We highlight how these structures contribute to the weakening of atherosclerotic plaque stability, impaired endothelial barrier integrity, platelet activation, and the initiation of the coagulation cascade. We also discuss the modulating role of classic risk factors such as hypertension, dyslipidemia, and exposure to tobacco smoke, which may increase the formation or hinder the elimination of NETs/NENs. We also focus on the practical application of this knowledge: we present biomarkers associated with the presence of NETs/NENs (cfDNA, MPO–DNA complexes, CitH3, NE), which may be useful in diagnostics and risk stratification, and we discuss innovative therapeutic strategies. In addition to classic methods for indirectly inhibiting NET/NEN formation (antiplatelet, anti-inflammatory, and immunometabolic agents), we present experimental approaches aimed at their neutralization and removal (e.g., DNase I, elastase, and myeloperoxidase inhibitors). We pay particular attention to the context of cardiac and cardiac surgical procedures (Percutaneous Coronary Intervention-PCI, coronary artery bypass grafting-CABG), where rapid NET/NEN bursts can increase the risk of acute thrombotic complications. The overall evidence indicates that NETs/NENs represent an innovative and promising research and therapeutic target, allowing us to view cardiovascular diseases in a new light—as a dynamic interaction of inflammatory, atherosclerotic, and thrombotic processes. This opens up new possibilities in diagnostics, combination treatment and personalisation of therapy, although further research and standardization of detection methods remain necessary.

Hair mineral analysis (HMA) has emerged as a promising non-invasive method for assessing long-term exposure to trace elements and metals, potentially complementing traditional biochemical and clinical markers of cardiovascular risk. This review synthesizes current evidence on the relationships between hair elemental profiles and cardiovascular disease (CVD), with an emphasis on toxic metals (As, Hg, Pb, Cd, Ni, Al) and essential micronutrients (Mg, Mn, Zn, Cu, Fe, Cr, Li). The reviewed studies consistently show that patients with CVD exhibit elevated levels of toxic elements and reduced concentrations of protective ones, reflecting oxidative stress, inflammation, and endothelial dysfunction as mechanistic links. Methodologically, the review highlights inductively coupled plasma mass spectrometry (ICP-MS) with collision/reaction cell technology and microwave digestion as gold-standard analytical approaches, while underscoring the urgent need for harmonized protocols, validated washing procedures, and certified reference materials. The interpretation of HMA requires consideration of temporal dynamics, external contamination, and regional variability. Although current evidence supports the research utility of HMA, its clinical integration remains limited by the absence of reference ranges and prospective validation. HMA may hold future value in environmental risk stratification and primary prevention in exposed populations, but further standardization and large-scale longitudinal studies are necessary to define its diagnostic and prognostic relevance in cardiovascular medicine.

Coronary artery disease (CAD) is increasingly recognized as a thromboinflammatory disorder in which innate immune activation and coagulation are tightly coupled within the plaque microenvironment. Emerging single-cell and spatial technologies have refined this paradigm by demonstrating that these processes are not diffusely distributed but instead concentrated within discrete cellular niches. This narrative review critically evaluates mechanistic and translational studies integrating single-cell RNA sequencing, spatial transcriptomics, and ligand–receptor modeling to characterize cell–cell communication networks driving immunothrombosis in CAD. Converging evidence from single-cell and spatial studies indicates substantial heterogeneity among macrophages, neutrophils, and smooth muscle cells, with functionally distinct subpopulations contributing differentially to inflammation, matrix remodeling, and thrombogenicity. Spatial analyses further demonstrate that procoagulant and inflammatory programs converge in anatomically defined high-risk regions, particularly at the plaque shoulder and sites of endothelial dysfunction. However, whether these transcriptional states represent causal drivers or epiphenomena remains unresolved. Many insights are derived from murine models or dissociated tissues, raising concerns regarding translational relevance and loss of spatial context. Additionally, computational inference of intercellular communication remains indirect and requires functional validation. In conclusion, immunothrombosis in CAD should be interpreted as an emergent property of spatially organized cellular networks rather than a uniform inflammatory state. While these approaches identify candidate therapeutic nodes, their clinical translation and the central challenge is to distinguish causal regulatory nodes from transcriptional correlates generated by high-dimensional profiling.