Panvascular disease (PVD) is an emerging clinical concept that encompasses a spectrum of atherosclerotic conditions involving multiple major vascular beds, including the coronary, cerebral, peripheral, and valvular arteries. Although not formally recognized as a nosological entity, in this review, PVD is adopted as a conceptual framework to reflect the systemic nature of atherosclerosis affecting vascular territories supplying the heart, brain, and peripheral circulation. This perspective enables a more integrated understanding of disease processes across organ systems that are often studied in isolation. Lipoprotein(a) [Lp(a)] is a genetically regulated, low-density lipoprotein (LDL)-like particle that has garnered increasing attention as an independent pathogenic risk factor for PVD. Accumulating evidence from epidemiological, genetic, and mechanistic studies has confirmed the multifaceted role of Lp(a) in promoting atherogenesis, vascular calcification, inflammation, and thrombogenesis across multiple vascular beds. Elevated Lp(a) levels are associated with increased cardiovascular and cerebrovascular event risk, even after controlling for traditional risk factors. This review systematically outlines the structure, genetic determinants, and pathogenic mechanisms of Lp(a), and synthesizes current clinical evidence regarding its role in various PVD subtypes. The interactions between Lp(a) and traditional cardiovascular risk factors such as hypercholesterolemia, diabetes, and hypertension are explored in depth, highlighting their synergistic contributions to vascular injury and disease progression. Furthermore, sex-based differences in Lp(a)-associated risk, response to therapy, and biological behavior are discussed, providing insights into personalized cardiovascular risk stratification. In addition, the review summarizes current and emerging therapeutic strategies targeting Lp(a), including niacin, antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), and gene-editing technologies. These advances offer promising new avenues for reducing residual cardiovascular risk attributable to elevated Lp(a). In conclusion, viewing Lp(a)-associated pathology through the lens of PVD provides a comprehensive and unifying approach to understanding its systemic impact. This framework supports the development of integrated risk assessment tools and multi-targeted interventions, ultimately aiming to improve outcomes for patients with complex, multisite vascular involvement.

Background: With the increasing prevalence of prediabetes and diabetes, exploring dietary factors associated with prediabetes and diabetes has become a global health research priority. This study aimed to assess the relationship between dietary decanoic acid (DDA) intake and the risk of diabetes and prediabetes.Methods: Data from the National Health and Nutrition Examination Survey (NHANES) 2005–2016 included 11,477 adult participants. DDA intake was assessed through two 24-h dietary recalls and participants were grouped according to the diagnostic criteria for diabetes and prediabetes. Multivariate regression models were applied to analyze the relationship between DDA intake and diabetes and prediabetes, with subgroup analyses conducted to explore potential interactions.Results: Dietary decanoic acid intake was significantly negatively associated with the risk of diabetes. In the fully adjusted model, each 1 g/day increase in DDA intake was associated with a 19% reduction in the odds of developing diabetes from prediabetes (OR = 0.81, 95% CI: 0.68–0.96, p = 0.015) and this negative association was more pronounced in individuals with higher education level (P for interaction = 0.006). Compared with the DDA intake ≤0.18 g/day, DDA intake >0.58 g/day is related to reduced risk of progression to diabetes in prediabetic patients. However, the relationship between DDA intake and the risk of prediabetes was not statistically significant in the fully adjusted model (OR = 0.95, 95% CI: 0.84–1.07, p = 0.404).Conclusion: This study found that higher DDA intake may be associated with lower prevalence of diabetes among prediabetic population, and high education level strengthen this relationship.

Inflammatory Bowel Disease (IBD), which includes Crohn’s disease and ulcerative colitis, is associated with an increased risk of Acute Myocardial Infarction (AMI). The genetic mechanisms underlying this link are not well understood. We downloaded IBD and AMI-related microarray datasets from the NCBI Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified and analyzed using enrichment analysis and Weighted Gene Co-expression Network Analysis (WGCNA). Machine learning techniques, including LASSO, random forest, and Boruta, were employed to screen for hub genes. These genes were validated through qRT-PCR and Western blotting. Single-cell sequencing was used to confirm findings. Additionally, potential therapeutic targets were identified using the Connectivity Map (CMap) database. Five key hub genes—THBD, FOSB, ADGPR3, IL1R2, and PLAUR—were identified as significantly involved in both IBD and AMI pathogenesis. A diagnostic model for AMI constructed using these hub genes demonstrated high predictive accuracy. Single-cell sequencing analysis and several potential drugs targeting these hub genes were identified, offering new therapeutic avenues. This study highlights the crucial role of FOSB and other hub genes in the comorbidity of IBD and AMI. The findings provide novel insights for early diagnosis and potential therapeutic strategies, emphasizing the importance of further investigation into these genetic links.

Non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio (NHHR) has demonstrated significant clinical application potential in the evaluation of vascular-related diseases. Our objective was to explore the impact of NHHR on the progression from prediabetes to diabetes or the regression to normal fasting glucose (NFG). This study utilized data from the first and third waves of the China Health and Retirement Longitudinal Study, involving 2922 participants. Based on the changes in glycemic status during the follow-up period, the outcome variables were categorized into three categories: progression to diabetes, persistence in prediabetes status, or return to NFG. Multivariable logistic regression analyses, restricted cubic spline regression analyses, stratification analyses, and sensitivity analyses were used to assess the effect of NHHR on the development of prediabetes. In a follow-up study spanning approximately three years, we observed that 558 participants (19.1%) returned to normal blood glucose levels, while 514 participants (17.6%) progressed to diabetes. After adjusting for potential confounding factors, we found a linear negative relationship between NHHR and the reversion from prediabetes to NFG [(odds ratio (OR) 0.88, 95% confidence interval (CI) 0.80–0.98)]. Additionally, NHHR exhibited a linear positive association with the progression from prediabetes to diabetes (OR 1.28, 95% CI 1.15–1.41). Stratified analyses revealed no significant interactions between NHHR and the subgroup variables. NHHR is significantly associated with prediabetes development in middle-aged and older adults. Lower NHHR levels increase the likelihood of prediabetes regression, whereas higher NHHR levels elevate the risk of prediabetes progression.