Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?
Atherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, a significant residual risk is still relevant, and is related to unmet therapeutic targets. Endothelia...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-01-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/2/1086 |
| _version_ | 1797441629517250560 |
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| author | Giovanni Ciccarelli Stefano Conte Giovanni Cimmino Patrizia Maiorano Andrea Morrione Antonio Giordano |
| author_facet | Giovanni Ciccarelli Stefano Conte Giovanni Cimmino Patrizia Maiorano Andrea Morrione Antonio Giordano |
| author_sort | Giovanni Ciccarelli |
| collection | DOAJ |
| description | Atherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, a significant residual risk is still relevant, and is related to unmet therapeutic targets. Endothelial dysfunction and lipid infiltration are the primary causes of atherosclerotic plaque progression. In this contest, mitochondrial dysfunction can affect arterial wall cells, in particular macrophages, smooth muscle cells, lymphocytes, and endothelial cells, causing an increase in reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and intracellular lipid deposition. The detection and characterization of mitochondrial DNA (mtDNA) is crucial for assessing mitochondrial defects and should be considered the goal for new future therapeutic interventions. In this review, we will focus on a new idea, based on the analysis of data from many research groups, namely the link between mitochondrial impairment and endothelial dysfunction and, in particular, its effect on atherosclerosis and aging. Therefore, we discuss known and novel mitochondria-targeting therapies in the contest of atherosclerosis. |
| first_indexed | 2024-03-09T12:25:52Z |
| format | Article |
| id | doaj.art-8a9bff649483488c9b7820f1b6ce418f |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-09T12:25:52Z |
| publishDate | 2023-01-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-8a9bff649483488c9b7820f1b6ce418f2023-11-30T22:35:11ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-01-01242108610.3390/ijms24021086Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?Giovanni Ciccarelli0Stefano Conte1Giovanni Cimmino2Patrizia Maiorano3Andrea Morrione4Antonio Giordano5Vanvitelli Cardiology Unit, Monaldi Hospital, 80131 Naples, ItalyDepartment of Translational Medical Sciences, Section of Lung Diseases, University of Campania “Luigi Vanvitelli”, 80131 Naples, ItalyVanvitelli Cardiology Unit, Monaldi Hospital, 80131 Naples, ItalySbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USASbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USASbarro Institute for Cancer Research and Molecular Medicine, Center of Biotechnology, College of Science and Technology, Temple University, Philadelphia, PA 19122, USAAtherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, a significant residual risk is still relevant, and is related to unmet therapeutic targets. Endothelial dysfunction and lipid infiltration are the primary causes of atherosclerotic plaque progression. In this contest, mitochondrial dysfunction can affect arterial wall cells, in particular macrophages, smooth muscle cells, lymphocytes, and endothelial cells, causing an increase in reactive oxygen species (ROS), leading to oxidative stress, chronic inflammation, and intracellular lipid deposition. The detection and characterization of mitochondrial DNA (mtDNA) is crucial for assessing mitochondrial defects and should be considered the goal for new future therapeutic interventions. In this review, we will focus on a new idea, based on the analysis of data from many research groups, namely the link between mitochondrial impairment and endothelial dysfunction and, in particular, its effect on atherosclerosis and aging. Therefore, we discuss known and novel mitochondria-targeting therapies in the contest of atherosclerosis.https://www.mdpi.com/1422-0067/24/2/1086mitochondrial disordersatherosclerosisendotheliumcardiovascular diseasecoronaryaging |
| spellingShingle | Giovanni Ciccarelli Stefano Conte Giovanni Cimmino Patrizia Maiorano Andrea Morrione Antonio Giordano Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? International Journal of Molecular Sciences mitochondrial disorders atherosclerosis endothelium cardiovascular disease coronary aging |
| title | Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? |
| title_full | Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? |
| title_fullStr | Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? |
| title_full_unstemmed | Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? |
| title_short | Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis? |
| title_sort | mitochondrial dysfunction the hidden player in the pathogenesis of atherosclerosis |
| topic | mitochondrial disorders atherosclerosis endothelium cardiovascular disease coronary aging |
| url | https://www.mdpi.com/1422-0067/24/2/1086 |
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