Decoding vascular aging: implications for atherosclerosis progression and clinical intervention

Age-related pathologies, particularly cardiovascular disorders, pose a significant global health concern. The World Health Organization (WHO) predicts an increase in advanced mortality by 2030 unless critical interventions are implemented. Atherosclerosis remains the major cause of various cardiovas...

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Main Authors: Silumbwe Ceaser Wankumbu, Xiao-Man Ji, Ming Xu
Format: Article
Language:English
Published: Open Exploration 2024-08-01
Series:Exploration of Drug Science
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Online Access:https://www.explorationpub.com/uploads/Article/A100856/100856.pdf
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author Silumbwe Ceaser Wankumbu
Xiao-Man Ji
Ming Xu
author_facet Silumbwe Ceaser Wankumbu
Xiao-Man Ji
Ming Xu
author_sort Silumbwe Ceaser Wankumbu
collection DOAJ
description Age-related pathologies, particularly cardiovascular disorders, pose a significant global health concern. The World Health Organization (WHO) predicts an increase in advanced mortality by 2030 unless critical interventions are implemented. Atherosclerosis remains the major cause of various cardiovascular diseases. Hence, this review focused on the interaction between known mechanisms of vascular aging, disease manifestation, and progression during atherosclerosis. In the review, we highlighted five altered vascular mechanisms in cardiovascular models: genomic instability, neurohormonal deregulation, epigenetics, protein regulation, and the gut microbiome. The articles were selected from various indexed scientific databases. It is important to note that the mechanisms are equally interrelated with other aging pathways, such as inflammation and senescence. In conclusion, atherosclerosis is multifaceted and cholesterol-lowering therapy has been widely used. However, more than one specific action line is required to eradicate or slow down its manifestation. Equally, establishing a balance between aging stressors resulting in vascular injuries and stress buffering mechanisms during aging is critical to the treatment of atherosclerosis. The promising therapeutic targets reviewed include the angiotensin (1–7)/MAS axis, the gut microbiome, histone deacetylases, DNA repair systems, noncoding RNAs, β3/dopamine adrenoceptors, senescence and inflammation checkpoints.
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spelling doaj-art-ca39a7a98dee4fb5932ce5a3561ae96b2025-02-08T03:30:12ZengOpen ExplorationExploration of Drug Science2836-76772024-08-012444947210.37349/eds.2024.00056Decoding vascular aging: implications for atherosclerosis progression and clinical interventionSilumbwe Ceaser Wankumbu0https://orcid.org/0000-0002-9071-4212Xiao-Man Ji1https://orcid.org/0009-0003-5199-2118Ming Xu2https://orcid.org/0000-0002-0655-2610Department of Clinical Pharmacy, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu, ChinaDepartment of Clinical Pharmacy, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu, ChinaDepartment of Clinical Pharmacy, School of Basic Medicine and Clinical Pharmacy, China Pharmaceutical University, Nanjing 210009, Jiangsu, ChinaAge-related pathologies, particularly cardiovascular disorders, pose a significant global health concern. The World Health Organization (WHO) predicts an increase in advanced mortality by 2030 unless critical interventions are implemented. Atherosclerosis remains the major cause of various cardiovascular diseases. Hence, this review focused on the interaction between known mechanisms of vascular aging, disease manifestation, and progression during atherosclerosis. In the review, we highlighted five altered vascular mechanisms in cardiovascular models: genomic instability, neurohormonal deregulation, epigenetics, protein regulation, and the gut microbiome. The articles were selected from various indexed scientific databases. It is important to note that the mechanisms are equally interrelated with other aging pathways, such as inflammation and senescence. In conclusion, atherosclerosis is multifaceted and cholesterol-lowering therapy has been widely used. However, more than one specific action line is required to eradicate or slow down its manifestation. Equally, establishing a balance between aging stressors resulting in vascular injuries and stress buffering mechanisms during aging is critical to the treatment of atherosclerosis. The promising therapeutic targets reviewed include the angiotensin (1–7)/MAS axis, the gut microbiome, histone deacetylases, DNA repair systems, noncoding RNAs, β3/dopamine adrenoceptors, senescence and inflammation checkpoints.https://www.explorationpub.com/uploads/Article/A100856/100856.pdfatherosclerosisinflammationvascular mechanismscardiovascular diseasestherapeutic targets
spellingShingle Silumbwe Ceaser Wankumbu
Xiao-Man Ji
Ming Xu
Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
Exploration of Drug Science
atherosclerosis
inflammation
vascular mechanisms
cardiovascular diseases
therapeutic targets
title Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
title_full Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
title_fullStr Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
title_full_unstemmed Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
title_short Decoding vascular aging: implications for atherosclerosis progression and clinical intervention
title_sort decoding vascular aging implications for atherosclerosis progression and clinical intervention
topic atherosclerosis
inflammation
vascular mechanisms
cardiovascular diseases
therapeutic targets
url https://www.explorationpub.com/uploads/Article/A100856/100856.pdf
work_keys_str_mv AT silumbweceaserwankumbu decodingvascularagingimplicationsforatherosclerosisprogressionandclinicalintervention
AT xiaomanji decodingvascularagingimplicationsforatherosclerosisprogressionandclinicalintervention
AT mingxu decodingvascularagingimplicationsforatherosclerosisprogressionandclinicalintervention