| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Topical Review |
1 Department of Molecular & Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130-3932, USA
There is abundant evidence that links hypercholesterolaemia to both vascular inflammation and atherogenesis. While atherosclerosis is a large vessel disease that is characterized by leucocyte infiltration and lipid deposition in the wall of lesion-prone arteries, the inflammatory response does not appear to be confined to these locations. There is evidence supporting a systemic inflammatory response that is characterized by endothelial cell activation in multiple vascular beds and the appearance of activated immune cells and a wide range of inflammatory mediators in blood. The mechanism(s) responsible for initiating this systemic response remain poorly defined, although several inciting factors have been proposed, including infectious agents and oxidative stress resulting from one or more of the cardiovascular risk factors (e.g. hypercholesterolaemia, hypertension). While cells within lesion-prone arteries are often inferred as the source of circulating inflammatory mediators during atherogenesis, the fact that endothelial cells throughout the vasculature are activated raises the possibility that the microvasculature (which encompasses a vast endothelial surface area) may contribute to creating the systemic inflammatory milieu that is linked to atherogenesis. This review addresses evidence that links the microvasculature to the inflammatory responses induced by hypercholesterolaemia and offers the hypothesis that inflammatory events initiated within the microcirculation may contribute to initiation and/or progression of large vessel disease.
(Received 19 November 2004;
accepted after revision 14 December 2004;
first published online 16 December 2004)
Corresponding author D. N. Granger: Department of Molecular & Cellular Physiology, LSU Health Sciences Center, 1501 Kings Highway, Shreveport, LA 71130-3932, USA. Email: dgrang{at}lsuhsc.edu
This article has been cited by other articles:
|
|
 |
|
  A. Tailor, K. C. Wood, J. L. Wallace, R. D. Specian, and D. N. Granger Roles of platelet and endothelial cell COX-1 in hypercholesterolemia-induced microvascular dysfunction Am J Physiol Heart Circ Physiol, December 1, 2007; 293(6): H3636 - H3642. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Klement, B. St. Croix, C. Milsom, L. May, Q. Guo, J. L. Yu, P. Klement, and J. Rak Atherosclerosis and Vascular Aging as Modifiers of Tumor Progression, Angiogenesis, and Responsiveness to Therapy Am. J. Pathol., October 1, 2007; 171(4): 1342 - 1351. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Zamir, R. Goswami, D. Salzer, and J. K. Shoemaker Cardiovascular Control: Role of vascular bed compliance in vasomotor control in human skeletal muscle Exp Physiol, September 1, 2007; 92(5): 841 - 848. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Y. Stokes NAD(P)H oxidase: where there's smoke, there's fire Am J Physiol Heart Circ Physiol, January 1, 2007; 292(1): H119 - H120. [Full Text] [PDF]
|
|
|
|
 |
|
 A. S. Damazo, S. Yona, R. J. Flower, M. Perretti, and S. M. Oliani Spatial and Temporal Profiles for Anti-Inflammatory Gene Expression in Leukocytes during a Resolving Model of Peritonitis J. Immunol., April 1, 2006; 176(7): 4410 - 4418. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
