The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress
The formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2022-11-01
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| Series: | Frontiers in Cardiovascular Medicine |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1042729/full |
| _version_ | 1811231344824418304 |
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| author | Bradley Field Bale Amy Lynn Doneen Pierre P. Leimgruber Pierre P. Leimgruber David John Vigerust |
| author_facet | Bradley Field Bale Amy Lynn Doneen Pierre P. Leimgruber Pierre P. Leimgruber David John Vigerust |
| author_sort | Bradley Field Bale |
| collection | DOAJ |
| description | The formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and inflammation becomes chronic and detrimental, resulting in atherosclerosis. When entrapment ceases, the association between lipids and inflammation is temporary and healthy, and the atherogenic process halts. Therefore, the link between lipids and inflammation depends upon lipoprotein retention in the intima. The entrapment is due to electrostatic forces uniting apolipoprotein B to polysaccharide chains on intimal proteoglycans. The genetic transformation of contractile smooth muscle cells in the media into migratory secretory smooth muscle cells produces the intimal proteoglycans. The protein, platelet-derived growth factor produced by activated platelets, is the primary stimulus for this genetic change. Oxidative stress is the main stimulus to activate platelets. Therefore, minimizing oxidative stress would significantly reduce the retention of lipoproteins. Less entrapment decreases the association between lipids and inflammation. More importantly, it would halt atherogenesis. This review will analyze oxidative stress as the critical link between lipids, inflammation, and the pathogenesis of atherosclerosis. Through this perspective, we will discuss stopping oxidative stress to disrupt a harmful association between lipids and inflammation. Numerous therapeutic options will be discussed to mitigate oxidative stress. This paper will add a new meaning to the Morse code distress signal SOS-stopping oxidative stress. |
| first_indexed | 2024-04-12T10:42:37Z |
| format | Article |
| id | doaj.art-6f6962b16fe34d249194fe9d1a9116da |
| institution | Directory Open Access Journal |
| issn | 2297-055X |
| language | English |
| last_indexed | 2024-04-12T10:42:37Z |
| publishDate | 2022-11-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj.art-6f6962b16fe34d249194fe9d1a9116da2022-12-22T03:36:32ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2022-11-01910.3389/fcvm.2022.10427291042729The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stressBradley Field Bale0Amy Lynn Doneen1Pierre P. Leimgruber2Pierre P. Leimgruber3David John Vigerust4Department of Medical Education and Clinical Sciences, Washington State University College of Medicine, Spokane, WA, United StatesDepartment of Medical Education and Clinical Sciences, Washington State University College of Medicine, Spokane, WA, United StatesDepartment of Medical Education and Clinical Sciences, Washington State University College of Medicine, Spokane, WA, United StatesDepartment of Medical Education and Clinical Sciences, University of Washington School of Medicine, Seattle, WA, United StatesDepartment of Neurological Surgery, Vanderbilt University School of Medicine, Nashville, TN, United StatesThe formation of an atheroma begins when lipoproteins become trapped in the intima. Entrapped lipoproteins become oxidized and activate the innate immune system. This immunity represents the primary association between lipids and inflammation. When the trapping continues, the link between lipids and inflammation becomes chronic and detrimental, resulting in atherosclerosis. When entrapment ceases, the association between lipids and inflammation is temporary and healthy, and the atherogenic process halts. Therefore, the link between lipids and inflammation depends upon lipoprotein retention in the intima. The entrapment is due to electrostatic forces uniting apolipoprotein B to polysaccharide chains on intimal proteoglycans. The genetic transformation of contractile smooth muscle cells in the media into migratory secretory smooth muscle cells produces the intimal proteoglycans. The protein, platelet-derived growth factor produced by activated platelets, is the primary stimulus for this genetic change. Oxidative stress is the main stimulus to activate platelets. Therefore, minimizing oxidative stress would significantly reduce the retention of lipoproteins. Less entrapment decreases the association between lipids and inflammation. More importantly, it would halt atherogenesis. This review will analyze oxidative stress as the critical link between lipids, inflammation, and the pathogenesis of atherosclerosis. Through this perspective, we will discuss stopping oxidative stress to disrupt a harmful association between lipids and inflammation. Numerous therapeutic options will be discussed to mitigate oxidative stress. This paper will add a new meaning to the Morse code distress signal SOS-stopping oxidative stress.https://www.frontiersin.org/articles/10.3389/fcvm.2022.1042729/fulloxidative stressplatelet-derived growth factorsmooth muscle cell transformationproteoglycansremnant cholesterollipoprotein retention |
| spellingShingle | Bradley Field Bale Amy Lynn Doneen Pierre P. Leimgruber Pierre P. Leimgruber David John Vigerust The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress Frontiers in Cardiovascular Medicine oxidative stress platelet-derived growth factor smooth muscle cell transformation proteoglycans remnant cholesterol lipoprotein retention |
| title | The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress |
| title_full | The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress |
| title_fullStr | The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress |
| title_full_unstemmed | The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress |
| title_short | The critical issue linking lipids and inflammation: Clinical utility of stopping oxidative stress |
| title_sort | critical issue linking lipids and inflammation clinical utility of stopping oxidative stress |
| topic | oxidative stress platelet-derived growth factor smooth muscle cell transformation proteoglycans remnant cholesterol lipoprotein retention |
| url | https://www.frontiersin.org/articles/10.3389/fcvm.2022.1042729/full |
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