Search Results (881)

High Mobility Group ^{Box 1} (HMGB1) and S100 proteins are major ligands of Receptor for Advanced Glycation End-products (RAGE) and have causal roles in endometriosis lesions. Yet the AGE–RAGE pathway that unifies Advanced Glycation End-products (AGEs) with these ligands has not been assessed in endometriosis. In diabetes, atherosclerosis, and chronic kidney disease, AGE–RAGE links insulin resistance and oxidative stress to inflammation, fibrosis, and organ harm. Endometriosis shares key drivers of AGE accumulation, including insulin resistance, oxidative stress, and chronic inflammation. Endometriosis is also linked to higher vascular risk and arterial stiffness. We asked whether AGE–RAGE could bridge metabolic stress to pelvic lesions and systemic risk. We did a focused review of mechanisms and an evidence map of studies on AGEs, RAGE, or known RAGE ligands in endometriosis. We grouped findings as most consistent with a driver, amplifier, consequence, or parallel role. We included 29 studies across human samples, cell systems, and animal models. Few studies measured AGE adducts directly. Most work tracked RAGE ligands (mainly HMGB1 and S100 proteins) and downstream immune and angiogenic programs. Across models, this pattern fits best with a self-reinforcing loop after lesions form. RAGE expression often aligned with lesion remodeling, especially fibrosis. Blood and skin readouts of AGE burden were mixed and varied by cohort and sample type. A central gap is receptor proof. Many models point to shared Toll-like receptor 4 (TLR4)/ nuclear factor kappa B (NF-κB) signaling, but few test RAGE dependence. Overall, current evidence supports AGE–RAGE as a disease-amplifying loop involved in chronic inflammation and fibrosis rather than an initiating trigger. Its effects likely vary by stage and site. Priorities now include direct lesion AGE measurement, paired systemic–pelvic sampling over time, receptor-level studies, and trials testing diet or drug interventions against clear endpoints. Outcomes could include fibrosis, angiogenesis, immune state, pain, and oocyte and follicle function. Full article

The liver plays a central role in numerous physiological processes, with one of its most critical functions being the regulation of lipid homeostasis through both the biogenesis and secretion of very low-density lipoproteins (VLDLs) and fatty acid oxidation. By forming and secreting VLDLs, the liver mitigates the influx of potentially toxic free fatty acids from the bloodstream and repurposes them for energy utilization throughout the body. Fatty acid oxidation is equally essential for maintaining hepatic lipid balance, and its disruption can lead to lipid accumulation and metabolic dysfunction-associated steatotic liver disease (MASLD), previously referred to as non-alcoholic fatty liver disease (NAFLD). Even subtle alterations in these processes can have profound health consequences, contributing to chronic liver diseases and atherosclerosis—the leading cause of cardiovascular morbidity and mortality worldwide. Despite their importance, many aspects of hepatic VLDL formation, secretion, and fatty acid oxidation remain poorly understood. This narrative review highlights the pivotal role of the liver in maintaining lipid balance, summarizes current knowledge on fatty acid uptake and processing, provides an in-depth analysis of VLDL biogenesis and secretion, and underscores the need for continued research in this critical area of human health. Full article

Cholesterol plays a fundamental role in the human body—it stabilizes cell membranes, modulates gene expression, and is a precursor to steroid hormones, vitamin D, and bile salts. Its correct level is crucial for homeostasis, while both excess and deficiency are associated with serious metabolic and health consequences. Excessive accumulation of cholesterol leads to the development of atherosclerosis, while its deficiency disrupts the transport of fat-soluble vitamins. Magnetic resonance spectroscopy (MRS) enables the detection of cholesterol esters and the differentiation between their liquid and crystalline phases, but the technical limitations of clinical MRI systems require the use of dedicated coils and sequence modifications. This study demonstrates the feasibility of using MRS to identify cholesterol-specific spectral signatures in atherosclerotic plaque through ex vivo analysis. Using a custom-designed experimental coil adapted for small-volume samples, we successfully detected characteristic cholesterol peaks from plaque material dissolved in chloroform, with spectral signatures corresponding to established NMR databases. To further enhance spectral quality, a deep-learning denoising framework based on a 1D U-Net architecture was implemented, enabling the recovery of low-intensity cholesterol peaks that would otherwise be obscured by noise. The trained U-Net was applied to experimental MRS data from atherosclerotic plaques, where it significantly outperformed traditional denoising methods (Gaussian, Savitzky–Golay, wavelet, median) across six quantitative metrics (SNR, PSNR, SSIM, RMSE, MAE, correlation), enhancing low-amplitude cholesteryl ester detection. This approach substantially improved signal clarity and the interpretability of cholesterol-related resonances, supporting more accurate downstream spectral assessment. The integration of MRS with NMR-based lipidomic analysis, which allows the identification of lipid signatures associated with plaque progression and destabilization, is becoming increasingly important. At the same time, the development of high-resolution techniques such as μOCT provides evidence for the presence of cholesterol crystals and their potential involvement in the destabilization of atherosclerotic lesions. In summary, nanotechnology-assisted MRI has the potential to become an advanced tool in the proof-of-concept of atherosclerosis, enabling not only the identification of cholesterol and its derivatives, but also the monitoring of treatment efficacy. However, further clinical studies are necessary to confirm the practical usefulness of these solutions and their prognostic value in assessing cardiovascular risk. Full article

Carotid atherosclerosis remains one of the primary etiological factors underlying ischemic stroke, contributing to adult neurological disability and mortality. In recent years, non-coding RNAs (ncRNAs) have emerged as key regulators of gene expression, actively modulating molecular pathways involved in atherogenesis. This systematic review, the first to be exclusively focused on carotid atherosclerosis, aimed at synthesizing current findings on the differential expression of ncRNAs throughout the natural history of the disease, thus providing the first comprehensive attempt to delineate a stage-specific ncRNA expression profile in carotid disease. A comprehensive literature search was conducted in PubMed and Scopus databases in January 2025, following PRISMA guidelines. Original studies involving human subjects with carotid atherosclerosis, evaluating the expression of intracellular or circulating ncRNAs, were included and then categorized according to their association with cardiovascular risk factors, carotid intima-media thickness (cIMT), presence of atherosclerotic plaques, plaque vulnerability, clinical symptoms, and ischemic stroke. Out of 148 articles initially identified, 49 met the inclusion criteria and were analyzed in depth. Among the different classes of ncRNAs, microRNAs (miRNAs) were the most frequently reported as dysregulated, followed by circular RNAs (circRNAs) and long non-coding RNAs (lncRNAs). Notably, the majority of identified ncRNAs were implicated in key pathogenic mechanisms such as inflammatory signaling, vascular smooth muscle cell (VSMC) phenotypic modulation, and ABCA1-mediated cholesterol efflux. Collectively, the evidence underscores the association and possible involvement of ncRNAs in the initiation and progression of carotid atherosclerosis and its cerebrovascular complications. Their relative stability in biological fluids and cell-specific expression profiles highlight their strong potential as minimally invasive biomarkers and—possibly—novel therapeutic targets. Full article

Vascular endothelial injury is a key pathological characteristic of multiple diseases, such as atherosclerosis, stroke, and mastitis. Aspirin eugenol ester (AEE) has been confirmed to exert a significant protective effect on vascular endothelial injury. However, the universal action patterns and underlying mechanisms of AEE across different pathological scenarios have not been systematically elucidated. This study aimed to investigate the effect and mechanism of AEE in alleviating multiple vascular endothelial injury models. Nine vascular endothelial injury models were established by treating bovine aortic endothelial cells (BAECs), mouse aortic endothelial cells (MAECs), and human umbilical vein endothelial cells (Huvecs) with ethanol (EtOH), hydrogen peroxide (H₂O₂), and copper sulfate (CuSO₄), respectively. The protective effects of AEE were systematically evaluated via morphological observation, detection of inflammatory responses, and oxidative stress markers. Furthermore, metabolomics was employed to identify and analyze differentially expressed metabolites between the nine model groups and AEE groups. AEE exerted protective effects on all nine vascular endothelial injury models, inhibiting inflammation and oxidative stress induced by all inducers. Metabolomic analysis revealed that the differentially expressed metabolites modulated by AEE in most models were primarily enriched in lipid metabolism, amino acid metabolism, coenzyme biosynthesis, and other related pathways. AEE could improve vascular endothelial injury by upregulating antioxidant substance which included eicosapentaenoic acid (EPA), choline, coenzyme A (CoA), glutathione (GSH), catalase (CAT) and superoxide dismutase (SOD), as well as downregulating substances that cause endothelial oxidative damage, including phytosphingosine (PS), palmitic acid (PA), and arachidonic acid (AA). Full article

Background and Objectives: Obesity, heart failure (HF), and atherosclerosis have common pathways, including chronic inflammation, immune cells activation, and metabolic disturbances. These pathways often coexist and overlap, increasing cardiometabolic risk. Growth differentiation factor 15 (GDF-15) is an emerging cytokine linked to inflammation, oxidative stress, and metabolic dysregulation, which are common pathways between heart failure, obesity and atherosclerosis. Beyond its established prognostic value in cardiovascular diseases (CVD) and HF, recent evidence suggests that GDF-15 may also reflect subclinical atherosclerosis, potentially improving early risk stratification in obese and HF populations. The aim of this review is to synthesize current evidence on the association between GDF-15 and markers of subclinical atherosclerosis, and to evaluate whether GDF-15 may serve as an integrative biomarker reflecting shared cardiometabolic pathways. Materials and Methods: We conducted a systematic review following PRISMA recommendations registered by CRD420251267457 number on PROSPERO. PubMed, Embase, Scopus, and Web of Science were searched for human studies evaluating the correlation between markers of subclinical atherosclerosis and GDF-15 concentration. We excluded the studies not published in English, not involving human participants, and not meeting the inclusion criteria. We assessed the risk of bias using the Joanna Briggs Institute appraisal tool. Due to the heterogeneity of studies, a narrative synthesis was performed. Result: The review included 18 studies, which evaluated the association between GDF-15 and subclinical atherosclerosis markers, such as intima media thickness, coronary artery calcium score, ankle-brachial index, and atherosclerotic plaques. Studies included patients with metabolic disorders, chronic inflammatory diseases, HIV cohorts, and general population samples. Most of the studies reported that GDF-15 levels were associated with greater atherosclerotic burden; however, results were frequently influenced by confounders. Methodological limitations, such as limited or highly specified samples, cross-sectional designs, variability in atherosclerotic-imaging technique, and inconsistent adjustment for confounders, restrict generalization of the results. Conclusions: Current evidence supports GDF-15 as a biomarker integrating inflammatory and metabolic stress signals, indirectly linking obesity, HF and subclinical atherosclerosis. While current data supports its prognostic relevance, further studies are needed to confirm its clinical utility in routine assessment and preventive cardiovascular care. Full article

Current pharmacotherapies against atherosclerotic cardiovascular disease are associated with considerable residual risk, together with various adverse side effects. Nutraceuticals, such as resveratrol (RSV), with excellent safety profile, represent promising alternatives and potential treatment. However, the full spectrum of anti-atherogenic actions regulated by RSV and the underlying molecular mechanisms remain poorly understood. The objective of this study therefore was to investigate the impact of RSV on key atherosclerosis-associated processes in monocytes, macrophages, endothelial cells, and smooth muscle cells in vitro, as well as in LDL receptor-deficient mice fed a high-fat diet in vivo. RSV produced beneficial changes in the plasma lipid profile and peripheral blood lymphoid cells in vivo. RSV also attenuated plaque inflammation by decreasing macrophage and T cell content and enhanced markers of plaque stability, with increased levels of smooth muscle cells and collagen content. In vitro, RSV inhibited chemokine-driven monocyte migration, inflammasome activation, matrix metalloproteinase activity, pro-inflammatory gene expression, reactive oxygen species production, and smooth muscle cell invasion. RNA-sequencing of the thoracic aorta revealed key genes and pathways mediating the antioxidant, anti-inflammatory and plaque-stabilising activities of RSV. These studies provide novel mechanistic insights on the anti-atherogenic actions of RSV and support further evaluation in human clinical trials. Full article

Atherosclerosis seriously endangers human health. Quercetin has drawn attention for its potential anti-atherosclerotic pharmacological effects. This study aimed to comprehensively assess quercetin’s effect and potential mechanism in treating atherosclerosis through a systematic review and meta-analysis. Preclinical studies published before 20 January 2025 were searched for in databases including PubMed, Embase, Web of Science, CNKI, Wanfang, and VIP. The CAMARADES list was used to assess the quality of the included studies. Stata 12 was applied for overall effect, sensitivity, subgroup, and publication bias analyses. Time–dose interval analyses were conducted to explore how quercetin dose and dosing cycle affect intervention effects. Finally, trial sequential analyses were performed using TSA 0.9 software. A total of 22 studies involving 421 animals were included, with a mean methodological quality score of 7.73/10. Meta-analysis showed that relative to the control group, quercetin reduced aortic plaque area, adjusted lipids (lowered TC, TG, and LDL-C and raised HDL-C), downregulated adhesion factors (e.g., VCAM-1) and pro-inflammatory factors (e.g., IL-1β and IL-6), upregulated anti-inflammatory factor IL-10 and antioxidant enzymes (SOD, CAT) while decreasing MDA content, and regulated atherosclerosis-related targets (e.g., LXRα, SIRT1, and mTOR). Subgroup analyses found model establishment time and quercetin administration time affected aortic lesion areas, TC, and TG. Time–dose analysis indicated quercetin had better ameliorative effects on atherosclerosis at 25–100 mg/kg with an 8–10-week intervention. Quercetin significantly improves atherosclerosis and inhibits its occurrence and progression through multiple pathways, such as regulating lipid metabolism, anti-inflammatory effects, and counteracting oxidative stress. Based on current evidence, quercetin is a potential therapeutic agent for treating atherosclerosis. Full article

(1) Cancer has been shown to contribute to the progression of atherosclerosis, while inflammatory aspects of atherosclerosis can exert profound effects on cancer development and outcomes. TA-MUC1 (Tumour-associated Mucin 1) is a transmembrane glycoprotein that is overexpressed in many human epithelial cancers lining the intestine. Interestingly, the lack of intestinal MUC1 has been shown to impair cholesterol uptake in MUC1^−/− mice. (2) To investigate whether TA-MUC1 could have specific effects on cholesterol metabolism and, thereby, have the potential of impacting the pathogenesis of atherosclerosis in cancer patients. (3) The effect of TA-MUC1 on cholesterol and lipid metabolism was assayed using MUC1 gene knock down breast cancer cells. An in vitro coculturing model similar to in vivo biological conditions was used to determine that TA-MUC1 could also modulate the cholesterol metabolism of other cells. (4) Reduction or inhibition of TA-MUC1 activity resulted in a significant alteration in a number of the signalling pathways and proteins that are relevant to abnormal cholesterol metabolism (p < 0.0001). Coculturing of TA-MUC1 cancer cells with THP-1 cells also notably effectively induced monocytic THP-1 cell differentiation towards foam cells—foam cells being a characteristic feature of atherosclerotic blood vessels. (5) Previously, we found TA-MUC1 downregulation led to a reduction in procoagulant and prothrombotic properties of the cancer cells as well as modulation of the aberrant calcium signalling pathways of cancer cells. Taken together with these current results, this suggests that TA-MUC1 in cancer cells has multiple effects on cholesterol and lipid metabolism, which also impacts other cells in the cellular bioenvironment. TA-MUC1 could thereby act as an important pathogenic effector of atherosclerosis in cancer. These results can also be considered in respect of the therapeutic anti-MUC1 antibody, which was able to reduce the effect of TA-MUC1 on cholesterol metabolism. Modulation of cholesterol metabolism via targeting TA-MUC1 could, therefore, be of great benefit to cancer patients with atherosclerosis. Full article

Atherosclerosis, a leading cause of cardiovascular disease, is driven by a complex interplay of dyslipidemia, inflammation, and arterial plaque formation and progression. Animal models are indispensable to elucidate the pathogenesis and develop novel therapies. Rodent models are widely utilized due to their cost-effectiveness, reproducibility, and rapid disease progression. However, notable species differences exist in lipoprotein composition and lipid metabolism pathways. Mice and rats exhibit an HDL-dominant profile, whereas Syrian golden hamsters express cholesteryl ester transfer protein (CETP) and display a higher LDL fraction, but lower than that of humans, offering a model closer to human metabolically. Divergent CETP activity across species further complicates the translational relevance of the findings from these models for atherosclerosis and related metabolic disorders. This review systematically examines the key factors in rodent model selection and optimization, with consideration on the roles of sex and age. We focus on three commonly used and well-characterized rodent strains prone to atherosclerosis: C57BL/6J mice, Sprague-Dawley (SD) rats, Wistar rats, and golden hamsters. On Apoe^−/− or Ldlr^−/− backgrounds, male C57BL/6 mice, owing to their pronounced hypercholesterolemia and extended survival with high-fat diet, are preferentially used in late-stage plaque stability studies. In contrast, male SD or Wistar rats develop atherosclerosis slowly with limited lesion progression, while hamsters, despite their human-like lipid metabolism, exhibit substantial individual variability and lesions that typically arrest at early fatty streaks with poor reproducibility. Therefore, rats and hamsters are better suited for studies focusing on early disease mechanisms and human-mimetic lipid metabolism. Full article

Background: Asthma and atherosclerosis frequently coexist in clinical populations and share convergent immunometabolic pathways amplified by gut microbial dysbiosis. We propose the gut–lung–vascular axis as a unifying mechanistic framework connecting epithelial and endothelial inflammation providing a foundation for understanding shared inflammatory mechanisms beyond tissue-specific disease boundaries. Methods: A targeted narrative review systematically appraised clinical, experimental and multi-omics studies published over the last five years to delineate microbiota-driven pathways relevant to asthma and atherosclerosis. Particular emphasis was placed on specific microbial taxa, metabolite profiles and immunometabolic networks that connect gut dysbiosis with respiratory and cardiovascular dysfunction. Results: Across human and experimental cohorts, dysbiosis marked by depletion of short-chain fatty acids (SCFAs) producing taxa (Faecalibacterium, Roseburia, Bacteroides) and enrichment of pathobionts (Proteobacteria, Haemophilus, Moraxella, Streptococcus) promotes epithelial and endothelial barrier dysfunction, amplifying Th2/Th17-skewed inflammation and endothelial injury. Key metabolites, including SCFAs, trimethylamine N-oxide (TMAO), secondary bile acids (BA), indole/tryptophan derivatives and lipopolysaccharides (LPS), serve as molecular connectors linking gut, airway and vascular inflammation. Microbial signatures and metabolomic patterns hold emerging diagnostic and therapeutic potential, and several drug classes (e.g., statins, corticosteroids, proton-pump inhibitors (PPIs)) further modulate host–microbiota interactions. Conclusions: Shared microbial taxa and metabolite signatures in asthma and atherosclerosis support microbiota-mediated immune dysregulation along the gut–lung–vascular axis as a common pathogenic framework. Microbial and metabolite profiling may enable improved risk stratification and precise, microbiota-targeted therapies. Integrating microbiome-informed diagnostics and personalized interventions could help reduce systemic inflammation and the burden of these overlapping inflammatory diseases. Full article

Murine macrophages exposed to oxidized low-density lipoprotein (oxLDL) polarize into a distinct Mox phenotype characterized by impaired phagocytic and chemotactic function. Although implicated in atherosclerosis, this phenotype has not been confirmed in human macrophages. Drawing parallels to human tumor-associated macrophages, and in contrast to the murine cell response, we hypothesize that LDL/oxLDL induces a hybrid Mox-like state in human macrophages, marked by the simultaneous secretion of pro-inflammatory cytokines and anti-inflammatory factors, potentially exacerbating vascular inflammation and atherogenesis. To test this, THP-1 human monocytes were differentiated into resting macrophages, then polarized into M1-like and M2-like phenotypes, followed by treatment with native LDL, oxLDL, IL-6, or their combinations. ELISA results showed that oxLDL or LDL with IL-6 polarized resting and M1-like macrophages into a Mox-like phenotype that secreted TNF-α and TGF-β1 at levels comparable to M1- and M2-like cells, respectively. The pro-inflammatory nature of Mox-like macrophages was supported by increased THP-1 adhesion to vascular endothelial cells exposed to the macrophage-conditioned media. In microfluidic assays, LUVA human mast cells migrated toward media from Mox-like macrophages, indicating enhanced chemotaxis. In summary, the pro-inflammatory Mox-like state is triggered in human macrophages by oxLDL or LDL combined with IL-6, a key regulator of the inflammatory acute-phase response. Unlike in murine cells, this state is marked by high chemotactic activity driven by TGF-β1 secretion, which promotes mast cell recruitment and contributes to atherosclerotic plaque development and Alzheimer’s disease. Full article

Porphyromonas gingivalis (P. gingivalis), a key periodontal pathogen, has been linked to atherosclerosis development. The clinical failure of antibiotics to improve cardiovascular outcomes necessitates alternative explanations. This study examines how sub-inhibitory concentrations of metronidazole affect the biogenesis and pathogenic potential of P. gingivalis extracellular vesicles (EVs) on human umbilical vein endothelial cells (HUVECs). EVs were isolated from both untreated bacteria (N-EVs) and those treated with sub-inhibitory concentrations of metronidazole (M-EVs) through ultracentrifugation. Characterization included transmission electron microscopy (TEM), nanoparticle tracking analysis, and Western blotting for virulence factors. HUVECs were evaluated using viability, migration, cell death assays, ROS detection, NF-κB activation imaging, and cytokine measurement. Sub-inhibitory concentrations of metronidazole increased EV production by 2.3-fold and enriched M-EVs with virulence factors (lipid A LPS, Kgp, RgpA). M-EVs demonstrated significantly stronger cytotoxicity, causing greater impairment of HUVEC viability and migration, alongside increased cell death. Mechanistically, M-EVs induced elevated mitochondrial and cellular ROS, promoting NF-κB activation and enhancing secretion of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Sub-inhibitory concentrations of metronidazole exacerbate endothelial injury by amplifying EV production and virulence factor loading in P. gingivalis, offering a mechanistic explanation for the limited cardiovascular benefits of antibiotic therapy in periodontitis patients. Full article

Citri grandis exocarpium (Citri grandis) has been consumed by human beings for fifteen hundred years. It is commonly consumed as a health drink and dietary supplement in China. However, its nutritional and healthcare functions are still not fully understood. Objective: Our previous study found that oral administration of Citri grandis extract can significantly decrease the blood lipid levels of hyperlipidemic mice fed a high-fat diet. The aim of this study was to confirm the preventative effects of Citri grandis extract against atherosclerosis. Methods: Atherosclerotic lesion models were induced in HUVECs and apoE^−/− C57BL/6J mice. ApoE^−/− mice fed a high-fat diet were orally administered Citri grandis extract (0.4, 0.8, and 1.6 g/kg/d BW) and Simvastatin (1 mg/kg/d BW) on the first day of model establishment. After a 16-week treatment, serum samples and aorta and liver tissues were collected. Observation of pathological changes in aortic and liver tissues was performed using a light microscope with oil red O, H&E, Masson’s trichrome staining, and TEM. Biochemical detection was employed to determine the serum levels of TC, TG, LDL-C, and HDL-C as well as the activities of AST and ALT. In addition, expression studies of TGF-β, PI3K, AKT1, PPAR-γ, LXR-α, and ABCA1 were performed via qPCR and Western blot analysis. Results: Compared with cholesterol-induced HUVECs, Citri grandis extract significantly enhanced cell viability, attenuated the morphological changes in HUVECs, and reduced LDH release. Furthermore, after treatment with Citri grandis extract, the levels of TC, TG, and LDL-C significantly decreased in the atherosclerosis model apoE^−/− mice after 16 weeks, and aortic plaque, lipid deposition, and endothelial injury were obviously ameliorated. The mRNA and protein expression of TGF-β, PPAR-γ, LXR-α, and ABCA1 in aortic and liver of atherosclerosis apoE^−/− mice were upregulated (p < 0.05, p < 0.01), while those of PI3K and Akt1 were suppressed (p < 0.05, p < 0.01). Conclusions: Citri grandis extract can significantly decrease the high circulating lipid levels and the liver lipid deposition of high-fat-diet-fed apoE^−/− mice and reduce aorta lipid accumulation and atherosclerotic plaques by regulating the expression of TGF-β1, PI3K, AKT1, PPAR-γ, LXR-α, and ABCA1. Citri grandis extract can be used as a healthcare dietary supplement for the prevention of abnormal lipid metabolism and atherosclerosis. Full article

Background: Vaspin (also known as serpinA12) is a recent discovery among adipokines. It plays a significant role in obesity-related conditions, many of which are classified as chronic, inflammatory or lifestyle diseases. Due to its anti-inflammatory and insulin-sensitizing properties, vaspin has been investigated as a biomarker and potential therapeutic agent. Methods: A literature review was conducted using the MEDLINE and SCOPUS databases using the phrases “vaspin” and “serpinA12” to summarize the most recent and influential research concerning vaspin’s mechanisms and influence on various tissues. Results and Conclusions: Vaspin is notably involved in metabolic syndrome, and it is generally associated with mitigating conditions like insulin resistance and obesity-related chronic inflammation. In addition, its beneficial effects on endothelial and smooth muscle cells under hyperglycemic and hyperlipidemic conditions are also well documented. There is growing evidence that vaspin positively impacts cardiovascular health, reducing the risk of ischemic stroke and the development of atherosclerosis. Moreover, some studies suggest a direct influence of vaspin on the central nervous system, with its administration shown to reduce the expression of neuropeptide Y, a key regulator of food intake. Many of the reviewed sources highlight vaspin not only as a possible biomarker but also as a promising therapeutic candidate. However, despite intensive research on vaspin over the past 20 years, there are significant disparities between animal and in vitro studies versus human studies. A further limitation in the field is the lack of standardization in research methodologies, which contributes to inconsistent and sometimes contradictory results. Full article