Lipids represent a valuable target for metabolomic studies since altered lipid metabolism is known to drive the pathological changes in cardiovascular disease (CVD). Metabolomic technologies give us the ability to measure thousands of metabolites providing us with a metabolic fingerprint of individual patients. Metabolomic studies in humans have supported previous findings into the pathomechanisms of CVD, namely atherosclerosis, apoptosis, inflammation, oxidative stress, and insulin resistance. The most widely studied classes of lipid metabolite biomarkers in CVD are phospholipids, sphingolipids/ceramides, glycolipids, cholesterol esters, fatty acids, and acylcarnitines. Technological advancements have enabled novel strategies to discover individual biomarkers or panels that may aid in the diagnosis and prognosis of CVD, with sphingolipids/ceramides as the most promising class of biomarkers thus far. In this review, application of metabolomic profiling for biomarker discovery to aid in the diagnosis and prognosis of CVD as well as metabolic abnormalities in CVD will be discussed with particular emphasis on lipid metabolites.

The pathophysiology of stoke involves many complex pathways and risk factors. Though there are several ongoing studies on stroke, treatment options are limited, and the prevalence of stroke is continuing to increase. Understanding the genomic variants and biological pathways associated with stroke could offer novel therapeutic alternatives in terms of drug targets and receptor modulations for newer treatment methods. It is challenging to identify individual causative mutations in a single gene because many alleles are responsible for minor effects. Therefore, multiple factorial analyses using single nucleotide polymorphisms (SNPs) could be used to gain new insight by identifying potential genetic risk factors. There are many studies, such as Genome-Wide Association Studies (GWAS) and Phenome-Wide Association Studies (PheWAS) which have identified numerous independent loci associated with stroke, which could be instrumental in developing newer drug targets and novel therapies. Additionally, using analytical techniques, such as meta-analysis and Mendelian randomization could help in evaluating stroke risk factors and determining treatment priorities. Combining SNPs into polygenic risk scores and lifestyle risk factors could detect stroke risk at a very young age and help in administering preventive interventions.

Vascular diseases, such as hypertension, atherosclerosis, cerebrovascular, and peripheral arterial diseases, present major clinical and public health challenges, largely due to their common underlying process: vascular remodeling. This process involves structural alterations in blood vessels, driven by a variety of molecular mechanisms. The inhibitor of DNA-binding/differentiation-3 (ID3), a crucial member of ID family of transcriptional regulators, has been identified as a key player in vascular biology, significantly impacting the progression of these diseases. This review explores the role of ID3 in vascular remodeling, emphasizing its involvement in processes such as apoptosis, cell proliferation, and extracellular matrix regulation. Furthermore, we examine how oxidative stress, intensified by exposure to estrogenic endocrine disruptors (EEDs) like polychlorinated biphenyls (PCBs) and bisphenol A (BPA), affects ID3 activity and contributes to vascular disease. Understanding the interaction between ID3 signaling and EED exposure provides critical insights into the molecular mechanisms underlying vascular remodeling and its role in the development and progression of vascular diseases.

Vascular diseases, including peripheral arterial disease (PAD), pulmonary arterial hypertension, and atherosclerosis, significantly impact global health due to their intricate relationship with vascular remodeling. This process, characterized by structural alterations in resistance vessels, is a hallmark of heightened vascular resistance seen in these disorders. The influence of environmental estrogenic endocrine disruptors (EEDs) on the vasculature suggests a potential exacerbation of these alterations. Our study employs an integrative approach, combining data mining with bioinformatics, to unravel the interactions between EEDs and vascular remodeling genes in the context of PAD. We explore the molecular dynamics by which EED exposure may alter vascular function in PAD patients. The investigation highlights the profound effect of EEDs on pivotal genes such as ID3, LY6E, FOS, PTP4A1, NAMPT, GADD45A, PDGF-BB, and NFKB, all of which play significant roles in PAD pathophysiology. The insights gained from our study enhance the understanding of genomic alterations induced by EEDs in vascular remodeling processes. Such knowledge is invaluable for developing strategies to prevent and manage vascular diseases, potentially mitigating the impact of harmful environmental pollutants like EEDs on conditions such as PAD.

Dietary factors play an important role in shaping the gut microbiome which, in turn, regulates the molecular events in colonic mucosa. The composition and resulting metabolism of the gut microbiome have been implicated in the development of colorectal cancer (CRC). Diets low in dietary fibers and phytomolecules as well as other lifestyle-related factors may predispose to CRC. Emerging evidence demonstrates that the predominance of microbes, such as Fusobacterium nucleatum, can predispose the colonic mucosa to malignant transformation. Dietary and lifestyle modifications have been demonstrated to restrict the growth of potentially harmful opportunistic organisms. In this study, we aim to present evidence regarding the relationship of dietary factors to the gut microbiome and development of CRC.

Background: Studies have shown that COVID-19 could lead coagulation defects, resulting in increased morbidity and mortality. In this study, we sought to estimate the prevalence of deep vein thrombosis (DVT) among COVID-19 hospitalizations and its effects on hospital outcomes using a large administrative database. Methods: We conducted a retrospective analysis of the 2020 California State Inpatient Database. All hospitalizations ≥18 years and primary diagnosis of COVID-19 were included and were stratified into those with and without DVT. The main outcomes of the study were in-hospital mortality, prolonged length of stay, vasopressor use, mechanical ventilation, and intensive care unit admission. Results: We included a total of 94,114 primary COVID-19 hospitalizations for the analysis. Among them, 1575 (1.7%) had DVT. After adjusting for covariates, regression analysis showed that those with DVT had significantly greater odds for mortality (adjusted odds ratio [aOR], 2.34; 95% confidence interval [CI], 2.07–2.65), prolonged length of stay (aOR, 3.51; 95% CI, 3.16–3.91), vasopressor use (aOR, 4.23; 95% CI, 3.78–4.74), mechanical ventilation (aOR, 2.90; 95% CI, 2.38–3.53), and intensive care unit admission (aOR, 4.32; 95% CI, 3.85–4.84). Conclusions: In our cohort, though only a few COVID-19 hospitalizations had DVT, the risk for adverse outcome was significantly higher. Therefore, healthcare providers should promptly monitor for DVT among COVID-19 patients and manage it promptly.