Current Atherosclerosis Reports最新文献

Purpose of review: Most observational studies quantify the relationship between diet, cardiovascular disease (CVD), and environmental impacts independently, resulting in a fragmented understanding of sustainable diets. This review summarizes findings from observational studies assessing eating patterns and their simultaneous associations with environmental and CVD outcomes.

Recent findings: Plant-based diets, primarily those low in red meat, added sugars, and sodium, are associated with lower CVD risks. Environmental studies suggest that whole-food diets low in animal proteins typically have a lesser impact on greenhouse gas emissions (GHGe) and land use than diets high in animal proteins; however, they may increase water use. Predominantly plant-based diets were consistently associated with lower cardiovascular risk and reduced environmental impacts, though trade-offs were observed between healthiness and environmental sustainability, as well as across different environmental indicators. Further research is needed to determine how dietary patterns, cardiovascular health, and environmental outcomes align.

Purpose of review: This review aims to summarize the current understanding of the regulatory mechanisms of nuclear factor of activated T cells c4 (NFATc4) in the pathogenesis of metabolic dysfunction-associated fatty liver disease (MAFLD). We focus on the multifaceted roles of NFATc4 in lipid metabolism, oxidative stress, inflammation, and insulin resistance, with the goal of evaluating its potential as a therapeutic target for MAFLD.

Recent findings: Emerging evidence indicates that NFATc4 is significantly upregulated in MAFLD patients and animal models. It promotes hepatic steatosis by inhibiting PPARα-mediated fatty acid oxidation, enhances oxidative stress via mitochondrial dysfunction, exacerbates inflammation through cytokine regulation and immune cell activation, and contributes to insulin resistance by modulating adipokine expression. Pharmacological inhibition of NFATc4 has shown protective effects in preclinical models, highlighting its therapeutic potential. NFATc4 serves as a critical transcriptional regulator in the progression of MAFLD, influencing multiple pathological processes through its nuclear translocation and interaction with key metabolic and inflammatory pathways. Targeting NFATc4 may offer a promising strategy for the treatment of MAFLD, though further research is needed to elucidate cell-type-specific mechanisms and develop tissue-specific inhibitors.

Purpose of review: Type 2 diabetes mellitus (T2DM) affects millions of adults worldwide and is associated with a 2 to 4-fold increased risk of cardiovascular disease, the leading cause of morbidity and mortality in this population. Traditional risk assessment tools have limitations in capturing the heterogeneity of cardiovascular risk among T2DM patients, prompting extensive research into novel biomarkers for enhanced risk stratification.

Recent findings: Recent evidence demonstrates that imaging, circulating, and body composition biomarkers have emerged as strong predictors of renal and cardiovascular outcomes allowing for further refinement in risk stratification. Coronary artery calcium scoring, hepatic steatosis, cardiac steatosis, and pericardial fat volume, provide superior prognostic value compared to conventional risk factors alone. Likewise, N-terminal pro-B-type natriuretic peptide (NT-proBNP), high-sensitivity troponin T, and inflammatory markers, have demonstrated independent prognostic value in this population. Lastly, anthropometric and body composition measures such as waist-to-hip ratio and visceral adiposity indices have emerged as stronger predictors of cardiovascular outcomes than body mass index. Moreover, T2DM treatment has evolved to prioritize cardiovascular and renal protection given recent landmark trials showed that specific new therapies, such as sodium-glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1), provide benefits independent of glycemic effects. Research has shown that some well-known as well as newly released biomarkers could guide therapy choice with the goal of providing optimal therapy to T2DM patients.  The aim of this paper is to examine how current imaging, body composition, and laboratory biomarkers can guide treatment decisions for T2DM, focusing on which altered biomarker profiles indicate the preferential use of specific pharmacotherapies.

Purpose of the review: The number of master athletes (MAs) is steadily increasing, reflecting broader societal trends in healthy aging and competitive sports participation beyond the age of 35. This work presents an up-to-date, evidence-based framework for evaluating the cardiovascular and general health of master athletes, integrating current guidelines with sport-specific considerations, and focusing primarily on cardiovascular prevention and risk management. It also acknowledges conditions that are more prevalent in this population-accelerated coronary calcification/coronary artery disease, endurance-related atrial fibrillation, and mild aortic enlargement-within the preventive assessment framework.

Recent findings: While regular exercise confers significant cardiovascular and metabolic benefits, aging athletes present unique clinical challenges requiring tailored assessment and management strategies. Current evidence highlights the importance of recognizing both traditional and sport-specific risk factors, employing appropriate diagnostic modalities (including advanced imaging when indicated), and implementing an integrated approach combining lifestyle, pharmacological, and procedural interventions. MAs require individualized, multidisciplinary care to ensure safe and sustained participation in sports. Early detection and targeted management of cardiovascular and metabolic risk factors, along with ongoing surveillance, are essential for preserving health, performance, and quality of life in this growing population.

Purpose of review: In this paper we review recent advancements in the diagnosis and management of atrial fibrillation through machine learning (ML).

Recent findings: Machine learning models developed from clinical records, electrocardiograms (ECGs) as well as data from implantable and wearable devices can now detect and even predict new-onset atrial fibrillation. Other models have improved prediction of stroke risk, increased the success of electrical cardioversions and facilitated catheter ablation of AF. Machine learning presents exciting new opportunities to enhance detection and management of atrial fibrillation. However, these developments need to be weighed against considerations of generalizability, equity, and transparency of these models for real-world utilization in clinical practice. We suggest targeted approaches for evaluation and utilization of ML models to allow for informed clinical implementation.

Purpose of review: Atherosclerosis, an inflammatory disease of large arteries, is a major cause of cardiovascular disease and stroke. Its pathogenesis involves complex interactions among endothelial cells, smooth muscle cells, macrophages, and other immune cells, forming atherosclerotic plaques. Secreted protein acidic and rich in cysteine (SPARC), a protein widely present in various cell types, participates in numerous biological processes. This review aims to explore the pathophysiologic role of SPARC in atherosclerosis and its significance in diagnosis and treatment.

Recent findings: Elevated expression of SPARC is observed in advanced atherosclerotic lesions and plasma concentrations of SPARC are higher in patients with ischemic cardiovascular disease. In a baboon model, SPARC expression correlates with LDL-C levels. However, the role and mechanism of SPARC in atherosclerosis remain to be explored. In this review, we elaborate on the critical roles of SPARC in endothelial dysfunction, macrophage polarization, smooth muscle cell proliferation, migration, and phenotypic transformation during the atherosclerotic process. The effects of SPARC on immune cells are also mentioned. Finally, we analyzed the potential of SPARC in the diagnosis and treatment of atherosclerosis.

Purpose of review: We synthesize the latest evidence (published 2020 to 2025) on the role of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in cardiovascular health, emphasizing biological mechanisms and key findings from observational studies and clinical trials related to cardiovascular disease (CVD) risk and outcomes.

Recent findings: EPA and DHA modulate lipid metabolism, inflammation, platelet and endothelial function, the gut-heart axis, ion channels and autonomic function via vagal tone, supporting cardiovascular health. While individual RCTs have produced variable results, updated cohort data and recent meta-analyses consistently link higher intake or circulating levels of EPA and DHA to reduced risk of cardiovascular events. However, evidence from RCTs indicates that high-dose supplementation may be associated with an increase in atrial fibrillation (AF) risk. Evidence supports a role for EPA and DHA in CVD prevention and treatment, with effects influenced by dose, formulation, and individual variability. Moderate intake appears safe and protective, while high dose EPA may offer added benefits in high-risk individuals but also might increase AF risk.

Purpose of review: This review aims to explore the epidemiology of lipoprotein(a) [Lp(a)] by its structural and genetic make-up variation amongst ancestry groups.

Recent findings: Lipoprotein(a) [Lp(a)] is a genetically determined lipoprotein particle, causally implicated in atherosclerotic cardiovascular disease (ASCVD) and calcific aortic valve stenosis (CAVS). Given its genetic basis, studies have shown marked ancestry-related differences in different races and ethnicities. Lp(a) plasma concentrations vary by more than 100-fold among individuals, primarily due to LPA gene polymorphisms and the number of kringle-IV type 2 (KIV2) repeats, which define apolipoprotein(a) [apo(a)] isoform size. Individuals of African descent have the highest median concentrations, followed by South Asians, with Hispanics/Latinos and East Asians having lower levels. Admixed populations display heterogeneity reflecting genetic ancestry. Despite differences in absolute levels, the relative ASCVD risk per unit increase in Lp(a) is consistent across groups, highlighting the universal atherogenicity of elevated Lp(a). Small apo(a) isoforms are associated with higher Lp(a) concentrations and risk, though isoform size is mainly a surrogate for Lp(a) burden. Despite a strong genetic basis and disproportionate burden in some populations, ancestry-specific testing guidelines are limited and testing rates remain low. Therapies targeting LPA transcription are in development, with outcome trials underway. Integrating ancestry-informed perspectives with universal risk principles is essential for equitable prevention and treatment. Routine, one-time Lp(a) testing enables cost-effective early risk stratification as Lp(a)-directed therapies emerge.

Purpose of review: The PI3K/Akt/mTOR (phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin) signaling pathway is pivotal in regulating cellular functions such as growth, proliferation, survival, and metabolism. Dysregulation of this pathway contributes to the pathogenesis of multiple diseases, including cancer, metabolic disorders, and cardiovascular diseases, notably atherosclerosis. This review outlines the role of the PI3K/Akt/mTOR pathway in the progression of atherosclerosis, emphasizing its involvement in endothelial protection, vascular smooth muscle cell proliferation and migration, as well as inflammatory modulation.

Recent findings: The pathway affects atherosclerosis through several mechanisms: it both protects and can harm the blood vessel lining, controls how muscle cells in vessel walls grow, move and die, and influences inflammation. These processes critically affect how plaques form, become unstable, and progress. Current drug treatments and procedures targeting this pathway show promise, though existing therapies often lack specificity. Understanding the many roles the PI3K/Akt/mTOR pathway plays in atherosclerosis offers important insights for creating targeted treatments. While current approaches show potential, we urgently need new interventions that specifically target this pathway to address heart disease complexity and improve patient results. Future studies should focus on developing more precise treatments to effectively reduce atherosclerosis.

Purpose of review: Cardiovascular-kidney-metabolic (CKM) syndrome involves complex interactions among cardiovascular, renal, and metabolic disorders. This review provides an overview of the mechanistic aspects of the epithelial-mesenchymal transition (EMT) and analyzes the regulatory impact of various statins on EMT-associated signaling pathways.

Recent findings: EMT and endothelial-to-mesenchymal transition (EndoMT) are crucial in the development of cardiac fibrosis, vascular remodeling, and interstitial fibrosis. Several signaling pathways, including the TGF-β/Smad, Wnt/β-catenin, MAPK, and Notch signaling pathways, as well as oxidative stress and inflammatory mediators, regulate these processes. Statins exert significant biological effects by downregulating proinflammatory cytokines, suppressing ROS, and inhibiting EMT-related signaling pathways. Statins can also inhibit EndoMT and reduce the progression of vascular fibrosis and atherosclerosis in the context of cardiovascular diseases. Similarly, in renal disorders such as chronic kidney disease (CKD) and diabetic nephropathy, statins reduce EMT in renal tubular epithelial cells by targeting pathways such as Smad and MAPK. CKM syndrome involves complex interactions among cardiovascular, renal, and metabolic disorders. Among the factors implicated in the pathophysiology of CKM, the EMT process is recognized as a key biological process. Evidence from preclinical and clinical studies supports the emerging role of statins as promising agents in managing CKM through modulating EMT. Therefore, understanding the diverse mechanisms of statins may lead to the development of more effective therapeutic strategies against CKM's fibrotic and inflammatory complications.