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Article: Age-Associated Arterial Remodelling

TitleAge-Associated Arterial Remodelling
Authors
KeywordsAge
Arterial Remodelling
Arteries
Collagen
Elastin
Issue Date2017
PublisherECronicon Open Access. The Journal's web site is located at https://www.ecronicon.com/cardiology.php
Citation
EC Cardiology, 2017, v. 4 n. 4, p. 137-164 How to Cite?
AbstractArterial remodelling is a major risk factor for a variety of age-related diseases and represents a potential target for therapeutic development. Blood vessel wall is continually remodelled at the tissue level as reflected by the changes in structure and functions. During ageing, the structural, mechanical and functional changes of arteries predispose individuals to the development of diseases related to vascular abnormalities in vital organs such as the brain, heart, eye and kidney. For example, aortic stiffness increases nonlinearly with advancing age - a few percent prior to 50 years of age but over 70% after 70 years of age. The elevated stiffness in large elastic arteries affects the blood pressure control and leads to increased transmission of high pressure to downstream smaller blood vessels, in turn affecting the microcirculation and end-organ functions. Meanwhile, the augmented remodelling of small arteries accelerates central arterial stiffening. This chapter is to provide an overview of age-associated changes in the arterial wall and their contributions to both central and peripheral vascular abnormalities associated with ageing. Therapeutics that specially target the different aspects of arterial remodelling are expected to be more effective than the traditional medications, particularly for the treatment and management of vascular ageing-related diseases.
Persistent Identifierhttp://hdl.handle.net/10722/261837

 

DC FieldValueLanguage
dc.contributor.authorMan, WCA-
dc.contributor.authorWang, Y-
dc.date.accessioned2018-09-28T04:48:57Z-
dc.date.available2018-09-28T04:48:57Z-
dc.date.issued2017-
dc.identifier.citationEC Cardiology, 2017, v. 4 n. 4, p. 137-164-
dc.identifier.urihttp://hdl.handle.net/10722/261837-
dc.description.abstractArterial remodelling is a major risk factor for a variety of age-related diseases and represents a potential target for therapeutic development. Blood vessel wall is continually remodelled at the tissue level as reflected by the changes in structure and functions. During ageing, the structural, mechanical and functional changes of arteries predispose individuals to the development of diseases related to vascular abnormalities in vital organs such as the brain, heart, eye and kidney. For example, aortic stiffness increases nonlinearly with advancing age - a few percent prior to 50 years of age but over 70% after 70 years of age. The elevated stiffness in large elastic arteries affects the blood pressure control and leads to increased transmission of high pressure to downstream smaller blood vessels, in turn affecting the microcirculation and end-organ functions. Meanwhile, the augmented remodelling of small arteries accelerates central arterial stiffening. This chapter is to provide an overview of age-associated changes in the arterial wall and their contributions to both central and peripheral vascular abnormalities associated with ageing. Therapeutics that specially target the different aspects of arterial remodelling are expected to be more effective than the traditional medications, particularly for the treatment and management of vascular ageing-related diseases.-
dc.languageeng-
dc.publisherECronicon Open Access. The Journal's web site is located at https://www.ecronicon.com/cardiology.php-
dc.relation.ispartofEC Cardiology-
dc.subjectAge-
dc.subjectArterial Remodelling-
dc.subjectArteries-
dc.subjectCollagen-
dc.subjectElastin-
dc.titleAge-Associated Arterial Remodelling-
dc.typeArticle-
dc.identifier.emailMan, WCA: andyman@hku.hk-
dc.identifier.emailWang, Y: yuwanghk@hku.hk-
dc.identifier.authorityWang, Y=rp00239-
dc.description.naturepublished_or_final_version-
dc.identifier.hkuros292267-
dc.identifier.volume4-
dc.identifier.issue4-
dc.identifier.spage137-
dc.identifier.epage164-
dc.publisher.placeUnited Kingdom-

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