Platelet-Rich Plasma in Cardiovascular Regeneration: Mechanistic Insights, Technological Innovations, and Future Directions.

Platelet-rich plasma (PRP), an autologous concentrate of platelets and bioactive molecules, has emerged as a promising regenerative therapy in cardiovascular medicine. The potential of PRP extends beyond hemostasis to include myocardial repair, angiogenesis, and immunomodulation. This review explores the biological mechanisms of PRP, its clinical applications in ischemic heart disease, peripheral artery disease, and inflammatory cardiopathies, and addresses challenges in standardization and translation. PRP exerts therapeutic effects through three primary mechanisms: promoting angiogenesis by stimulating endothelial cell proliferation and migration, exerting anti-inflammatory and immunomodulatory effects by balancing cytokine release, and enhancing myocardial repair and functional recovery by activating resident cardiac progenitor cells. Despite the promise of PRP, challenges such as variability in PRP composition due to differences in preparation methods and safety concerns remain. To overcome these barriers, precision engineering and cross-disciplinary integration are crucial. Innovations such as nanotechnology-driven targeted delivery systems and clustered regularly interspaced short palindromic repeats (CRISPR)-edited exosomes offer mechanism-specific interventions. Artificial intelligence (AI)-driven approaches utilizing single-cell RNA sequencing data can enable personalized treatment strategies, while closed-loop systems minimize batch-to-batch variability. Collaborative efforts between clinicians, engineers, and regulators are essential to establish global standards for exosome characterization. PRP-based therapies hold immense promise for revolutionizing cardiovascular regenerative medicine by modulating angiogenesis, inflammation, and myocardial repair. By embracing these advanced technologies and interdisciplinary approaches, PRP can transition from an empirical treatment to a data-driven, mechanism-specific intervention, ultimately redefining the future of cardiovascular care.