Panax ginseng Across the Cardiovascular Continuum: Molecular Targets, Mechanistic Convergence, and Translational Challenges

Cardiovascular diseases develop through an interconnected continuum that extends from cardiometabolic risk factors and vascular dysfunction to myocardial ischemic injury, pathological remodeling, and heart failure. Panax ginseng and its bioactive constituents have shown cardiovascular protective effects in various experimental models. However, the molecular mechanisms shared across different stages of the cardiovascular continuum remain insufficiently integrated. This review critically synthesizes current evidence on Panax ginseng, ginseng-derived constituents, and ginseng-containing preparations across major stages of cardiovascular disease. Particular emphasis is placed on convergent molecular networks involving metabolic and mitochondrial homeostasis, oxidative stress and inflammation, autophagy and mitophagy, regulated cell death, calcium handling, vascular and fibrotic remodeling, and gut microbiota–host interactions. Several target-oriented mechanisms, including peroxisome proliferator activated receptor (PPAR) γ, ryanodine receptor 2, histone acetyltransferase P300/dihydrolipoamide dehydrogenase/pyruvate dehydrogenase, Fas-associated death domain/PPARα, and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 2A-associated regulation, are highlighted and distinguished from pathway-level or phenotypic evidence. Despite extensive preclinical data, direct target engagement, causal validation, pharmacokinetic characterization, preparation standardization, and clinical evidence remain limited. Integrating target-level validation with standardized ginseng interventions and clinically relevant models may provide a stronger molecular basis for evaluating the cardiovascular potential of ginseng.