The Immunometabolic Architecture of Cardiovascular Disease: From Molecular Mechanisms to Precision Therapeutic Strategies
DOI:
https://doi.org/10.64229/z36aqk64Keywords:
Immunometabolic cardiovascular disease, Meta-inflammation mitochondrial dysfunction, SGLT2 inhibitors, Senolytics, Clonal hematopoiesis of indeterminate potential, Clonal genomic profilingAbstract
Cardiovascular diseases (CVDs) remain the leading cause of global mortality, yet traditional hemodynamic and lipid-centric models prove insufficient to capture the biological complexity driving residual cardiovascular risk. Converging evidence increasingly reframes CVD pathophysiology as a systemic immunometabolic disorder driven by the interplay of mitochondrial dysfunction, chronic immune activation, clonal hematopoiesis of indeterminate potential, and metabolic stress. This review critically synthesizes emerging paradigms in precision cardiovascular medicine, spanning molecular bioenergetics, epigenetic reprogramming, and immune-metabolic crosstalk within a unified immunometabolic-precision medicine framework, and evaluates translational advances including Sodium-glucose cotransporter-2 inhibitors, senolytics, and AI-driven risk stratification that directly target these mechanisms. Looking beyond current limitations, it appraises the transformative potential of multi-omics integration and regenerative engineering as the next frontier of cardiovascular precision medicine. By translating immunometabolic mechanisms into actionable clinical frameworks, this review argues for a paradigm shift: from reactive disease management toward precision-guided, biologically informed, and equitably accessible cardiovascular care.
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