The Possibility of Using Proteins as a Treatment of Atherosclerosis

Authors

  • Xinran Ma

DOI:

https://doi.org/10.54097/r0qh2c54

Keywords:

Atherosclerosis, prosaposin, HMG-CoA, protein treatment, macrophage.

Abstract

Atherosclerosis is a type of heart disease in which most patients either have coronary disease or carotid disease. Patients with atherosclerosis have narrowed blood vessels due to the formation of plaque or the condensation of fat molecules in the blood. The death rate from atherosclerosis is not extremely high, but atherosclerosis can easily lead to fatal diseases like heart attack and stroke. Atherosclerosis can be prevented by keeping a healthy lifestyle and taking medicines, and severe cases can be treated with surgeries. Protein treatment is not widely used for the treatment of atherosclerosis, but some proteins like prosaposin and HMG-CoA display their essential role in the synthesis of plaque. Prosaposin affects the inflammation of macrophages in the cell by affecting mTOR and S6K1 signaling passageways. Inflammation is the root cause of atherosclerosis, and decreasing inflammation can lead to a decrease in plaque. HMG-CoA is another protein that can affect cholesterol synthesis, which is crucial in plaque formation. HMG-CoA reductase inhibitor, which can be called statin, blocks the HMG-CoA from functioning and decreases the rate of cholesterol formation. The possibility of using prosaposin and HMG-CoA as a protein treatment is proven, and future experiments could determine the method to apply the treatment in clinical trials.

Downloads

Download data is not yet available.

References

Fan J, Watanabe T. Atherosclerosis: Known and unknown. Pathol Int. 2022 Mar; 72(3): 151-160. doi:10.1111/pin.13202. Epub 2022 Jan 25. PMID: 35076127.

John L, George A. K, Riitta S, Richard D. C, Jukka T. S. Socioeconomic Status and Carotid Atherosclerosis. Circulation. 1995; 92(7): 1786-1792. doi:10.1161/01.CIR.92.7.1786.

Fujiwara N, Kobayashi K. Macrophages in inflammation. Curr Drug Targets Inflamm Allergy. 2005 Jun; 4(3): 281-6.

Song B, Bie Y, Feng H, Xie B, Liu M, Zhao F. Inflammatory Factors Driving Atherosclerotic Plaque Progression New Insights. J Transl Int Med. 2022 Apr 2; 10(1): 36-47. doi:10.2478/jtim-2022-0012. PMID: 35702179; PMCID: PMC8997796.

Mandy M. T. van Leent et al., Prosaposin mediates inflammation in atherosclerosis. Sci. Transl. Med.13, eabe1433(2021). DOI:10.1126/scitranslmed.abe1433.

Jacob F B, Fumiyuki O, Renu V, Erling F. Mechanisms of Plaque Formation and Rupture. Circulation Research. 2014; 114(12): 1852-1866. doi:10.1161/CIRCRESAHA.114.302721.

Motta, M.; Tatti, M.; Salvioli, R. Autophagic dysfunction in Gaucher disease and its rescue by cathepsin B and D proteases. In Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging; Elsevier: Amsterdam, The Netherlands, 2014; pp. 131–146.

Matthias Nahrendorf Filip K. Swirski, Neutrophil-macrophage communication in inflammation and atherosclerosis. Science349, 237-238(2015). DOI:10.1126/science.aac7801.

Kabi A, McDonald C, 2014 Protein phosphatase 2A has positive and negative roles in autophagy, pp. 211–225 in Autophagy: Cancer, Other Pathologies, Inflammation, Immunity, Infection, and Aging. Elsevier, Amsterdam.

Shao, W.; Espenshade, P.J. Lipids. Cholesterol Synthesis and Regulation. In Encyclopedia of Biological Chemistry III; Elsevier: Amsterdam, The Netherlands, 2021; pp. 732–738. ISBN 978-0-12-822040-5.

Sakai K, Nagashima S, Wakabayashi T, Tumenbayar B, Hayakawa H, Hayakawa M, et al. Myeloid HMG-CoA (3-Hydroxy-3-Methylglutaryl-Coenzyme A) reductase determines Atherosclerosis by modulating migration of macrophages. Arterioscler. Thromb. Vasc. Biol. 2018; 38: 2590-2600.

Ucar M, Mjörndal T, Dahlqvist R. HMG-CoA reductase inhibitors and myotoxicity. Drug Saf. 2000 Jun; 22(6): 441-57. doi:10.2165/00002018-200022060-00003. PMID: 10877038.

Koushki K, Shahbaz SK, Mashayekhi K, Sadeghi M, Zayeri ZD, Taba MY, Banach M, Al-Rasadi K, Johnston TP, Sahebkar A. Anti-inflammatory Action of Statins in Cardiovascular Disease: the Role of Inflammasome and Toll-Like Receptor Pathways. Clin Rev Allergy Immunol. 2021 Apr; 60(2): 175-199. doi:10.1007/s12016-020-08791-9. PMID: 32378144; PMCID: PMC7985098.

Downloads

Published

29-12-2023