Advances in nanotechnology have opened new avenues for precision therapy, personalized medicine, and multifunctional theranostics in atherosclerosis (AS). This review provides a comprehensive overview of the role of nanoparticles (NPs) in precision medicine for AS, discussing their applications, challenges, and future prospects. The review first analyzes the current treatment landscape of AS and outlines potential biological targets for therapy. Various nanocarriers, including organic, inorganic, and hybrid systems, are evaluated for their therapeutic potential, with a focus on targeted drug delivery, anti-inflammatory therapy, vascular repair, plaque stabilization, and lipid clearance. Additionally, the review explores NP preparation methods, emphasizing strategies to enhance drug loading, stability, and controlled release. Finally, the translational challenges of NP-based therapies, including biocompatibility, large-scale production, regulatory hurdles, and clinical implementation, are critically analyzed. Future directions highlight the importance of interdisciplinary collaboration and technological innovation in advancing nanoparticle-based precision medicine for AS.

Heart failure (HF) is an end-stage cardiovascular syndrome caused by structural or functional cardiac abnormalities. Its high morbidity and mortality underscore the urgent need for novel therapeutic strategies. In recent years, the dynamic regulatory mechanisms underlying macrophage polarization in the onset and progression of HF have attracted widespread attention. The Sirtuin family, as NAD⁺ -dependent deacetylases, has emerged as a key regulatory factor in reshaping the macrophage polarization phenotype by integrating metabolic reprogramming, epigenetic regulation, and immune cell interactions. This paper systematically elaborates the molecular mechanisms by which Sirtuins (SIRT1-SIRT7) regulate metabolic reprogramming (e.g., glucose metabolism, lipid metabolism, and glutamine metabolism), coordinate epigenetic modifications (e.g., DNA methylation, histone modifications, and non-coding RNA regulation), and mediate interactions between immune cells to dynamically balance macrophage polarization. Furthermore, this review summarizes recent advances in the active components of phytomedicines, such as resveratrol, pterostilbene, astragaloside IV, quercetin, dihydromyricetin, berberine, honokiol, ginsenoside Rc, ginsenoside Rg1, and ginsenoside Rg3, in targeting the Sirtuin-macrophage polarization axis for the prevention and treatment of HF. This review aims to provide a theoretical framework and translational guidance for developing HF-targeted therapeutic strategies based on Sirtuin-mediated macrophage polarization, as well as for the research and development of related natural products.

Heart failure (HF) is a disease with high morbidity and mortality rates worldwide and significantly affects human health. Currently, the treatment options for HF are limited, and there is an urgent need to discover new therapeutic targets and strategies. Macrophages are innate immune cells involved in the development of HF. They play a crucial role in maintaining cardiac homeostasis and regulating cardiac stress. Recently, macrophages have received increasing attention as potential targets for treating HF. With the improvement of technological means, the study of macrophages in HF has made great progress. This article discusses the biological functions of macrophage phagocytosis, immune response, and tissue repair. The polarization, pyroptosis, autophagy, and apoptosis are of macrophages, deeply involved in the pathogenesis of HF. Modulation of the phenotypic changes of macrophages can improve immune-inflammation, myocardial fibrosis, energy metabolism, apoptosis, and angiogenesis in HF.

Rheumatoid arthritis (RA) is a systemic autoimmune condition that leads to chronic arthritis, disability, and reduced lifespan. Current therapies show limited effectiveness and often cause severe side effects, with up to 50% of patients discontinuing disease-modifying antirheumatic drugs (DMARDs) due to unsatisfactory outcomes. Natural bioactive compounds (NBCs), such as glycosides, alkaloids, terpenoids, flavonoids, polyphenols, and coumarins, have gained attention for their immunomodulatory and anti-inflammatory properties. However, challenges like poor solubility, high dosage requirements, short action duration, and low tissue specificity hinder their clinical use. Nanoparticle (NP)-based delivery systems, including lipid NPs (LNPs), polymer carriers, and inorganic nanocarriers, have been designed to address these challenges through passive, active, and stimuli-responsive strategies. NBC-loaded NPs target immune dysfunction, synovial hyperplasia, bone destruction, angiogenesis, inflammation, and oxidative stress (OS) in RA. This article highlights recent advancements in NBCs for RA treatment, nanoformulation design, and targeted mechanisms, while addressing challenges and future directions in this field. The integration of cutting-edge nanotechnology has demonstrated significant potential to overcome traditional barriers such as low bioavailability and off-target effects through intelligent NPs design. Future research should enhance artificial intelligence (AI)-driven modeling to predict drug-nanocarrier interactions, develop biomarker frameworks for precision nanomedicine, and optimize RA management.

Heart failure (HF) marks the culmination of numerous cardiac pathologies, presenting a major medical hurdle in prevention and treatment. In recent years, with the advancements in genomics and metabolomics, research has demonstrated that gut microbiota plays a significant role in the pathogenesis of HF. Trimethylamine N-oxide (TMAO) is a gut microbiota-derived metabolite and primarily sourced from foods abundant in choline, L-carnitine, and betaine. Research has shown that patients with HF exhibit higher levels of TMAO. Accumulating evidence has indicated that TMAO directly or indirectly mediates the occurrence and development of HF through multiple mechanisms. Furthermore, TMAO functions as a crucial prognostic marker in HF. Therefore, TMAO emerges as a potential therapeutic target for HF. This article reviews the generation and metabolic pathways of TMAO, emphasizes its pathophysiological mechanisms in HF, and explores promising therapeutic approaches targeting TMAO, offering novel insights and strategies for HF management.

Cardiovascular diseases remain the leading cause of death worldwide. Maladaptive transcriptional programs drive the fibrosis, hypertrophy, and vascular inflammation that characterize these pathologies. Histone posttranslational modifications regulate these programs by remodeling chromatin accessibility and transcriptional output in cardiomyocytes, vascular cells, and immune cells. These modifications include methylation, acetylation, and metabolite‐derived acylations. While the enzymatic machinery of classical histone marks is increasingly well defined, the cell‐type‐specific integration of these regulators into dynamic cardiovascular networks remains incompletely understood. This narrative review summarizes experimental and human studies published up to early 2026. We examine how classical marks such as H3K27me3 and H3K9ac, alongside emerging metabolic sensors like histone lysine lactylation, shape core pathobiological programs, including oxidative stress responses, endothelial dysfunction, and extracellular matrix remodeling, across major cardiovascular syndromes. We further critically evaluate the enzymatic machinery and pharmacological strategies by contrasting broad‐spectrum histone deacetylase inhibition with precision approaches, including bromodomain inhibition and locus‐selective epigenome editing. Finally, we address translational constraints such as drug delivery and off‐target effects. We propose that single‐cell resolution and spatial multiomics will be essential to identify compartment‐specific targets and advance precision cardiovascular epigenetic therapeutics.