Atherosclerosis is considered the major cause of morbidity and mortality in cardiovascular diseases (CVDs): This is a complex degenerative inflammatory and metabolic disease widely associated with genetic predisposition and multiple risk factors such as hypertensions, hyperlipidaemia and diabetes mellitus and is the main underlying cause of main CVDs [1].

Current therapies are mainly comprised of preventive treatments based on the levels of certain risk factors as cholesterol and blood pressure, smoking and so on [2]. Once the plaque is detected, the treatments usually consist of medications to lower cholesterol, such as statins, or medications to decrease the clotting, but a limited efficacy was detected when the drugs are administered systemically[3].

The present work proposes the evaluation of biomimetic artificial nanocells (ANs), that is, vesicles reconstructed from the whole cytoplasmic membranes of murine macrophages (RAW 264.7) using scalable and pharmaceutically applicable processes, retaining the composition, orientation and functions associated with cells membranes. In these ANs, the statin drug pravastatin was encapsulated to high extents, taking profit of the protection provided by the biomimetic nanocarrier as well as the targeting ability. Pravastatin-loaded ANs demonstrated to be a promising biomimetic drug delivery system for Atherosclerosis treatment, confirmed by their selective cell internalization, reduction of ox-LdL uptake and reactive oxygen species (ROS) production and increases in cholesterol efflux levels.

[1]       G.K. Hansson, Inflammation, Atherosclerosis, and coronary artery disease, New England Journal of medicine, 352(16): 1685-1695 (2005).

[2]       N. DiStasio, S. Lehoux, A. Khademhosseini, M. Tabrizian, The Multifaced Uses and Therapeutic Advantages of Nanoparticles for Atherosclerosis Research, Materials, 11(5): 754 (2018).

[3]       C. Gao, Q. Huang, C. Liu, C.H. Kwong, L. Yue, J. B. Wan, S.M. Lee, R. Wang., Treatment of atherosclerosis by macrophage-biomimetic nanoparticles via targeted pharmacotherapy and sequestration of proinflammatory cytokines, Nature communications, 11(1): 1 - 14 (2020).