Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness

Systemic inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD). How exactly inflammation leads to this is not fully understood, but it has been suggested that arterial stiffening, could provide potential mechanisms to explain it. Chronic, systemic inflammatory...

Full description

Bibliographic Details
Main Authors: Kaisa M. Mäki-Petäjä, Ian B. Wilkinson
Format: Article
Language:English
Published: BMC 2012-04-01
Series:Artery Research
Subjects:
Online Access:https://www.atlantis-press.com/article/125929731/view
_version_ 1811302499008643072
author Kaisa M. Mäki-Petäjä
Ian B. Wilkinson
author_facet Kaisa M. Mäki-Petäjä
Ian B. Wilkinson
author_sort Kaisa M. Mäki-Petäjä
collection DOAJ
description Systemic inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD). How exactly inflammation leads to this is not fully understood, but it has been suggested that arterial stiffening, could provide potential mechanisms to explain it. Chronic, systemic inflammatory conditions, as well as acute-models of inflammation are associated with arterial stiffening. Moreover, aortic stiffness can be reversed with successful immunomodulatory therapy. Although it seems evident that inflammation is involved in the process of aortic stiffening, the precise mechanism responsible for this remains unclear. There are number of possible mechanisms by which inflammation could lead to arterial stiffening. (1) Inflammation is associated with endothelial dysfunction and this can regulate arterial stiffness via changes in smooth muscle tone. (2) Inflammation leads to increased synthesis of matrix metalloproteinases, which can degrade elastin, resulting in stiffening. (3) Several mediators of inflammation may directly stimulate vascular calcification, whereas endogenous inhibitors of vascular calcification are downregulated during inflammation, both of which can lead to stiffening. (4) During inflammation arterial glycosaminoglycan (GAG) synthesis is upregulated. In animal models, an overproduction of certain GAGs in the aorta results in stiffening of the arterial wall by thinning of elastic lamellae. (5) Finally, direct vascular inflammation could lead to arterial stiffening by changing the composition of extracellular matrix. This review aims to discuss potential mechanisms by which inflammation could lead to aortic stiffening.
first_indexed 2024-04-13T07:29:11Z
format Article
id doaj.art-586d8e0c5b5a4bea84972c2743cb89ae
institution Directory Open Access Journal
issn 1876-4401
language English
last_indexed 2024-04-13T07:29:11Z
publishDate 2012-04-01
publisher BMC
record_format Article
series Artery Research
spelling doaj.art-586d8e0c5b5a4bea84972c2743cb89ae2022-12-22T02:56:24ZengBMCArtery Research1876-44012012-04-016210.1016/j.artres.2012.03.002Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffnessKaisa M. Mäki-PetäjäIan B. WilkinsonSystemic inflammatory conditions are associated with an increased risk of cardiovascular disease (CVD). How exactly inflammation leads to this is not fully understood, but it has been suggested that arterial stiffening, could provide potential mechanisms to explain it. Chronic, systemic inflammatory conditions, as well as acute-models of inflammation are associated with arterial stiffening. Moreover, aortic stiffness can be reversed with successful immunomodulatory therapy. Although it seems evident that inflammation is involved in the process of aortic stiffening, the precise mechanism responsible for this remains unclear. There are number of possible mechanisms by which inflammation could lead to arterial stiffening. (1) Inflammation is associated with endothelial dysfunction and this can regulate arterial stiffness via changes in smooth muscle tone. (2) Inflammation leads to increased synthesis of matrix metalloproteinases, which can degrade elastin, resulting in stiffening. (3) Several mediators of inflammation may directly stimulate vascular calcification, whereas endogenous inhibitors of vascular calcification are downregulated during inflammation, both of which can lead to stiffening. (4) During inflammation arterial glycosaminoglycan (GAG) synthesis is upregulated. In animal models, an overproduction of certain GAGs in the aorta results in stiffening of the arterial wall by thinning of elastic lamellae. (5) Finally, direct vascular inflammation could lead to arterial stiffening by changing the composition of extracellular matrix. This review aims to discuss potential mechanisms by which inflammation could lead to aortic stiffening.https://www.atlantis-press.com/article/125929731/viewAortic stiffnessInflammationRheumatoid arthritis
spellingShingle Kaisa M. Mäki-Petäjä
Ian B. Wilkinson
Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
Artery Research
Aortic stiffness
Inflammation
Rheumatoid arthritis
title Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
title_full Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
title_fullStr Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
title_full_unstemmed Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
title_short Inflammation and large arteries: Potential mechanisms for inflammation-induced arterial stiffness
title_sort inflammation and large arteries potential mechanisms for inflammation induced arterial stiffness
topic Aortic stiffness
Inflammation
Rheumatoid arthritis
url https://www.atlantis-press.com/article/125929731/view
work_keys_str_mv AT kaisammakipetaja inflammationandlargearteriespotentialmechanismsforinflammationinducedarterialstiffness
AT ianbwilkinson inflammationandlargearteriespotentialmechanismsforinflammationinducedarterialstiffness