Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease
Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood. Pu...
| Main Authors: | , |
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| Format: | Article |
| Language: | English |
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SAGE Publishing
2023-04-01
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| Series: | Clinical Medicine Insights: Cardiology |
| Online Access: | https://doi.org/10.1177/11795468231170779 |
| _version_ | 1797836763683618816 |
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| author | Emily Mewborn Ansley Stanfill |
| author_facet | Emily Mewborn Ansley Stanfill |
| author_sort | Emily Mewborn |
| collection | DOAJ |
| description | Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood. Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS. Conclusions: OS (primarily from excess reactive oxygen species) and inflammation are present along the entire ASCVD pathophysiologic continuum. An expanded list of clinical and social ASCVD risk factors (including hypertension, obesity, diabetes, kidney disease, inflammatory diseases, substance use, poor nutrition, psychosocial stress, air pollution, race, and genetic ancestry) influence ASCVD largely through increased OS. Many risk factors exert a positive feedback mechanism to increase OS. One genetic risk factor, haptoglobin (Hp) genotype, is associated with higher ASCVD risk in diabetes and hypothesized to do the same in those with insulin resistance due to the Hp 2-2 genotype increasing OS. Implications: Understanding the biological mechanisms of OS informs how these ASCVD risk factors relate to each other and compound ASCVD risk. Individualized ASCVD risk estimation should include a comprehensive, holistic perspective of risk factors to better address the clinical, social, and genetic influences of OS. Preventing and reducing OS is key to preventing ASCVD development or progression. |
| first_indexed | 2024-04-09T15:15:15Z |
| format | Article |
| id | doaj.art-9ee060b7a7484ddb8f7fd5dff15e58f9 |
| institution | Directory Open Access Journal |
| issn | 1179-5468 |
| language | English |
| last_indexed | 2024-04-09T15:15:15Z |
| publishDate | 2023-04-01 |
| publisher | SAGE Publishing |
| record_format | Article |
| series | Clinical Medicine Insights: Cardiology |
| spelling | doaj.art-9ee060b7a7484ddb8f7fd5dff15e58f92023-04-30T06:03:23ZengSAGE PublishingClinical Medicine Insights: Cardiology1179-54682023-04-011710.1177/11795468231170779Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular DiseaseEmily Mewborn0Ansley Stanfill1University of Tennessee Health Science Center, Memphis, TN, USADepartment of Genetics, Genomics, and Informatics, College of Medicine, University of Tennessee Health Science Center, Memphis, TN, USABackground: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood. Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS. Conclusions: OS (primarily from excess reactive oxygen species) and inflammation are present along the entire ASCVD pathophysiologic continuum. An expanded list of clinical and social ASCVD risk factors (including hypertension, obesity, diabetes, kidney disease, inflammatory diseases, substance use, poor nutrition, psychosocial stress, air pollution, race, and genetic ancestry) influence ASCVD largely through increased OS. Many risk factors exert a positive feedback mechanism to increase OS. One genetic risk factor, haptoglobin (Hp) genotype, is associated with higher ASCVD risk in diabetes and hypothesized to do the same in those with insulin resistance due to the Hp 2-2 genotype increasing OS. Implications: Understanding the biological mechanisms of OS informs how these ASCVD risk factors relate to each other and compound ASCVD risk. Individualized ASCVD risk estimation should include a comprehensive, holistic perspective of risk factors to better address the clinical, social, and genetic influences of OS. Preventing and reducing OS is key to preventing ASCVD development or progression.https://doi.org/10.1177/11795468231170779 |
| spellingShingle | Emily Mewborn Ansley Stanfill Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease Clinical Medicine Insights: Cardiology |
| title | Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease |
| title_full | Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease |
| title_fullStr | Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease |
| title_full_unstemmed | Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease |
| title_short | Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease |
| title_sort | oxidative stress underpins clinical social and genetic risk factors for atherosclerotic cardiovascular disease |
| url | https://doi.org/10.1177/11795468231170779 |
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