From 2010 to 2025, evidence increasingly identifies the gut microbiome, microbial dysbiosis, trimethylamine-N-oxide (TMAO), and short-chain fatty acids (SCFAs) as modulators of atherosclerosis and cardiovascular disease. We conducted a narrative review of literature retrieved from PubMed, Scopus, and the Clinical Trials Registry-India (CTRI), covering studies published between January 2010 and March 2025. A total of 103 primary studies (animal, n=15; human cohort, n=28; mechanistic, n=22; randomized controlled trials, n=38) and 10 ongoing clinical trials were reviewed. Germ-free and antibiotic-treated murine models support a role for TMA-producing microbial communities in plaque formation, whereas SCFA-producing communities attenuate inflammation and atherogenesis. In humans, elevated TMAO levels are associated with a 2-5-fold higher risk of major adverse cardiovascular events (MACE), although causal inference remains limited. Probiotics, synbiotics, dietary interventions, and fecal microbiota transplantation may improve TMAO, LDL cholesterol, and inflammatory markers, but definitive reductions in cardiovascular events have not been demonstrated. Overall, microbiome-targeted strategies remain promising but require large, diverse clinical trials to establish causality and clinical benefit.

To evaluate the cardioprotective effects of luteolin, a naturally occurring flavonoid, in mitigating critical pathological processes linked to cardiovascular diseases (CVDs), including oxidative stress, inflammation, mitochondrial dysfunction, and endothelial damage. Luteolin, found in celery, parsley, green peppers, and chamomile tea, exhibits significant cardioprotective properties through various mechanisms. It activates the Nrf2/HO-1 antioxidant pathway, suppresses NF-κB-mediated inflammation, regulates apoptosis, and preserves the functionality of endothelial nitric oxide synthase (eNOS). In preclinical studies involving isoproterenol- and doxorubicin-induced cardiotoxicity, luteolin was shown to reduce oxidative stress, decrease apoptosis, and improve cardiac structure and function. Compared to other flavonoids like quercetin and resveratrol, luteolin demonstrates more potent endothelial-protective effects and a balanced modulation of antioxidant and apoptotic pathways. The diverse actions and natural origin of luteolin make it a promising candidate for CVD prevention and as an adjunctive therapy. Future research should focus on rigorously designed clinical trials to validate its efficacy in heart failure, ischemic injury, and drug-induced cardiotoxicity, thus enhancing its application in clinical practice.

Pregnancy profoundly alters drug disposition through dynamic physiologic adaptations affecting absorption, distribution, metabolism, and excretion. Although pharmacogenomics has transformed precision therapeutics across multiple medical specialties, its application during pregnancy remains limited because conventional pharmacogenomic models assume stable genotype-phenotype relationships that do not account for the temporal biologic changes of gestation. This mini-review proposes a conceptual framework for obstetric-pharmacogenomics in which maternal, placental, and fetal-genomes interact within a continuously evolving physiologic environment to shape drug exposure, therapeutic efficacy, and toxicity. Pregnancy-induced alterations in cytochrome P450 enzyme activity, drug transporters, placental metabolism, and immune regulation may amplify, attenuate, or fundamentally modify genetically determined drug responses, rendering static pharmacogenomic classifications insufficient. We discuss the clinical implications of this dynamic paradigm across several therapeutic areas, including antiretroviral therapy, maternal mental health, hypertensive disorders of pregnancy, and analgesia, and highlight the need for trimester-specific approaches to individualized drug therapy. We further examine current barriers to implementation, including the exclusion of pregnant women from pharmacogenomic research, limited longitudinal data, and ethical considerations surrounding fetal genetics. Integrating pharmacogenomics with physiologically based pharmacokinetic modeling and multi-omics technologies offers an opportunity to redefine precision-medicine in obstetrics and advance safer, more effective, and individualized pharmacotherapy for pregnant-women and their offspring.

Dual antiplatelet therapy (DAPT), combining aspirin with a P2Y12 inhibitor, remains central to secondary prevention after acute coronary syndrome and percutaneous coronary intervention. However, substantial interindividual variability in antiplatelet response, particularly clopidogrel resistance associated with CYP2C19 polymorphisms, has challenged the conventional "one-size-fits-all" approach and increased interest in precision-guided antiplatelet strategies. This narrative review synthesized literature identified through PubMed, Scopus, Web of Science, and Google Scholar, focusing on randomized trials, genotype-guided studies, platelet function testing (PFT), meta-analyses, guideline statements, and emerging artificial intelligence (AI)-based prediction models. Evidence suggests that genotype-guided therapy, PFT-guided treatment, and individualized DAPT duration may improve the balance between ischemic protection and bleeding risk in selected high-risk populations. However, routine implementation remains limited by inconsistent clinical outcome benefits, heterogeneous testing strategies, modest risk-score performance, cost, infrastructure barriers, and variable guideline recommendations. Precision-guided DAPT is promising, but broader adoption requires stronger prospective evidence, standardized testing pathways, and real-world validation.

Gestational diabetes mellitus (GDM) is a common metabolic complication of pregnancy and is increasingly recognized as a marker of long-term metabolic vulnerability. Beyond its established association with cardiometabolic diseases, emerging epidemiological evidence suggests a potential link between GDM and increased cancer risk, particularly hormone-sensitive malignancies such as endometrial and breast cancer. This narrative review integrates epidemiological and mechanistic evidence exploring the relationship between GDM and long-term oncological susceptibility. Hyperglycemia, hyperinsulinemia, and chronic low-grade inflammation associated with GDM may contribute to proliferative signaling and metabolic dysregulation. Among the proposed mechanisms, insulin/IGF-1 signaling represents one of the most biologically plausible links, whereas pathways involving PI3K/Akt/mTOR activation, metabolic reprogramming, and tumor microenvironment alterations remain largely inferred from broader oncological literature. In addition, persistent metabolic stress during pregnancy may induce long-term epigenetic and immunometabolic changes potentially associated with carcinogenic susceptibility. Although current evidence does not establish a direct causal relationship between GDM and cancer, the integration of epidemiological and mechanistic findings supports the hypothesis that GDM may function as an early marker of systemic metabolic vulnerability associated with increased long-term oncological risk. Further longitudinal and mechanistic studies are needed to clarify this relationship and its clinical implications.