Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.

The rising epidemic of cardiovascular (CV) disease is fuelled by obesity, hypertension and diabetes and, independently and cumulatively, by an aging population. Extensive research identified immunoinflammatory mechanisms as key drivers in the initiation and progression of the disease, from early asy...

Full description

Bibliographic Details
Main Authors: Puntmann, V, Taylor, P, Mayr, M
Format: Journal article
Language:English
Published: 2011
_version_ 1797060258693120000
author Puntmann, V
Taylor, P
Mayr, M
author_facet Puntmann, V
Taylor, P
Mayr, M
author_sort Puntmann, V
collection OXFORD
description The rising epidemic of cardiovascular (CV) disease is fuelled by obesity, hypertension and diabetes and, independently and cumulatively, by an aging population. Extensive research identified immunoinflammatory mechanisms as key drivers in the initiation and progression of the disease, from early asymptomatic stages of vascular and myocardial injury leading to the clinically manifest dysfunction and remodeling in advanced stages. Underlying processes include endothelial dysfunction and extracellular matrix restructuration leading to increased vascular stiffness, as well as myocardial remodeling with dilatation and wall thinning. In this, overproduction of tumor necrosis factor-α, amongst others, contributes to generalized CV injury and dysfunction. Moreover, recent insights into the involvement of innate and adaptive immunity in atherosclerosis have shed light on many interesting parallels with chronic systemic inflammatory conditions, such as rheumatoid arthritis, with aggravated inflammation-induced vascular and myocardial injury. Besides, chronologic age has been identified as a potent, independent risk for reduced CV capacity and a plethora of heart diseases, with other modifiable risk factors acting as accelerators. We discuss the available evidence and propose that characterization of inflammatory CV responses might reveal a distinctive CV inflammatory phenotype. A comprehensive noninvasive bio-signature, comprising immunomic biomarkers and integrated noninvasive imaging, may serve as a potential tool in the early diagnosis and prognostication of CV risk.
first_indexed 2024-03-06T20:14:40Z
format Journal article
id oxford-uuid:2bbdafc9-632d-46e7-bd9d-b87a635fc827
institution University of Oxford
language English
last_indexed 2024-03-06T20:14:40Z
publishDate 2011
record_format dspace
spelling oxford-uuid:2bbdafc9-632d-46e7-bd9d-b87a635fc8272022-03-26T12:32:55ZCoupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:2bbdafc9-632d-46e7-bd9d-b87a635fc827EnglishSymplectic Elements at Oxford2011Puntmann, VTaylor, PMayr, MThe rising epidemic of cardiovascular (CV) disease is fuelled by obesity, hypertension and diabetes and, independently and cumulatively, by an aging population. Extensive research identified immunoinflammatory mechanisms as key drivers in the initiation and progression of the disease, from early asymptomatic stages of vascular and myocardial injury leading to the clinically manifest dysfunction and remodeling in advanced stages. Underlying processes include endothelial dysfunction and extracellular matrix restructuration leading to increased vascular stiffness, as well as myocardial remodeling with dilatation and wall thinning. In this, overproduction of tumor necrosis factor-α, amongst others, contributes to generalized CV injury and dysfunction. Moreover, recent insights into the involvement of innate and adaptive immunity in atherosclerosis have shed light on many interesting parallels with chronic systemic inflammatory conditions, such as rheumatoid arthritis, with aggravated inflammation-induced vascular and myocardial injury. Besides, chronologic age has been identified as a potent, independent risk for reduced CV capacity and a plethora of heart diseases, with other modifiable risk factors acting as accelerators. We discuss the available evidence and propose that characterization of inflammatory CV responses might reveal a distinctive CV inflammatory phenotype. A comprehensive noninvasive bio-signature, comprising immunomic biomarkers and integrated noninvasive imaging, may serve as a potential tool in the early diagnosis and prognostication of CV risk.
spellingShingle Puntmann, V
Taylor, P
Mayr, M
Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title_full Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title_fullStr Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title_full_unstemmed Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title_short Coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction: systemic inflammation and aging - a mini-review.
title_sort coupling vascular and myocardial inflammatory injury into a common phenotype of cardiovascular dysfunction systemic inflammation and aging a mini review
work_keys_str_mv AT puntmannv couplingvascularandmyocardialinflammatoryinjuryintoacommonphenotypeofcardiovasculardysfunctionsystemicinflammationandagingaminireview
AT taylorp couplingvascularandmyocardialinflammatoryinjuryintoacommonphenotypeofcardiovasculardysfunctionsystemicinflammationandagingaminireview
AT mayrm couplingvascularandmyocardialinflammatoryinjuryintoacommonphenotypeofcardiovasculardysfunctionsystemicinflammationandagingaminireview