The Role of 13-Hydroxyoctadecadienoic Acid, 15-Lipoxygenase, and Peroxisome Proliferator-Activated Receptor Alpha Gene Polymorphism (rs1800206) in Acute Coronary Syndrome: Pathophysiological Insights and Biomarker Relevance

Acute Coronary Syndrome (ACS) represents a spectrum of life-threatening cardiovascular conditions characterized by sudden myocardial ischemia. This review synthesizes current knowledge on the pathophysiological roles of 13-hydroxyoctadecadienoic acid (13-HODE), 15-lipoxygenase (15-LOX), and peroxisome proliferator-activated receptor alpha (PPAR-α) in ACS development, with particular emphasis on the PPAR-α rs1800206 (Leu162Val) polymorphism. Emerging evidence highlights the dual role of 13-HODE as both a pro-inflammatory mediator and angiogenic factor, while 15-LOX drives oxidative stress and contributes to plaque destabilization. The PPAR-α pathway emerges as a critical regulator of lipid metabolism and vascular inflammation, with the rs1800206 variant modifying disease susceptibility and therapeutic responses to fibrates. The authors further explore established and novel biomarkers, including high-sensitivity troponin, CK-MB, hs-CRP, and atherogenic lipid profiles, which collectively enhance ACS diagnosis and risk stratification. The integration of these molecular and genetic markers provides a framework for understanding the complex interplay between inflammation, oxidative stress, and metabolic dysregulation in ACS. Therefore, the findings have value in the clinic since they increase therapy choices for PPAR-α and draw attention to the potential for personalized medicine in ACS. This literature review endeavors to push precision medicine for ACS, by reviewing the specific mechanisms of 13-HODE, 15-LOX and PPAR-α polymorphisms and showing how this information can be applied to help patients.