Atherosclerosis is the leading cause of cardiovascular disease (CVD). Historically, the management of atherosclerosis was focused on decreasing lipid profile levels; however, recent evidence demonstrated that platelets and leukocytes play an important role in forming and exacerbating atherosclerosis. L-arginine (L-Arg), a precursor to nitric oxide (NO), plays a critical role in modulating oxidative stress and influencing platelet-leukocyte recruitment and has been extensively addressed in the context of CVD.
We aimed to perform a comprehensive literature review on L-Arg metabolism in the causative pathway of atherosclerosis compared to conventional treatment and it as a putative therapeutic approach.
L-Arg supplementation has shown promising effects on NO production, improving endothelial function and reducing oxidative stress in preclinical models. Clinical studies have indicated moderate improvements in vascular health markers, including reductions in inflammation and oxidative stress, although results have varied across studies. The potential of L-Arg to modify platelet-leukocyte recruitment and slow the progression of atherosclerotic plaque development has been observed in certain studies. However, these benefits remain inconsistent, and more robust clinical trials are needed to confirm its effectiveness. Additionally, while L-Arg appears to be relatively safe, some studies reported mild gastrointestinal discomfort as a common side effect.
L-Arg holds potential as a complementary or alternative treatment for atherosclerosis, particularly in improving endothelial function and reducing inflammation and oxidative stress. However, the variability in clinical outcomes and the lack of long-term data required further investigation into assessing therapeutic benefits. Future studies should focus on determining optimal dosing regimens, evaluating their long-term safety, and assessing their potential in combination with other therapies to enhance cardiovascular outcomes.