ATVB In Focus |
From the Department of Cell Biology, Section Immunology, Faculty of Medical Sciences, University of Groningen, The Netherlands.
Correspondence to J.L. Hillebrands, PhD, Department Cell Biology/Section Immunology, Faculty of Medical Sciences, University of Groningen, A. Deusinglaan 1, NL-9713 AV Groningen, The Netherlands. E-mail j.l.hillebrands{at}med.rug.nl
Abstract
To date, clinical solid-organ transplantation has not achieved its goals as a long-term treatment for patients with end-stage organ failure. Development of so-called chronic transplant dysfunction (CTD) is now recognized as the predominant cause of allograft loss long term (after the first postoperative year) after transplantation. CTD has the remarkable histological feature that the luminal areas of intragraft arteries become obliterated, predominantly with vascular smooth muscle cells (VSMCs) intermingled with some inflammatory cells (transplant arteriosclerosis, or TA). The development of TA is a multifactorial process, and many risk factors have been identified. However, the precise pathogenetic mechanisms leading to TA are largely unknown and, as a result, adequate prevention and treatment protocols are still lacking. This review discusses the origin (donor versus recipient, bone marrow versus nonbone marrow) of the VSMCs in TA lesions. Poorly controlled influx and subsequent proliferative behavior of these VSMCs are considered to be critical elements in the development of TA. Available data show heterogeneity when analyzing the origin of neointimal VSMCs in various transplant models and species, indicating the existence of multiple sites of origin. Based on these findings, a model considering plasticity of VSMC origin in TA in relation to severity and extent of graft damage is proposed.
Key Words: chronic transplant dysfunction transplantation transplant arteriosclerosis origin vascular smooth muscle cells
This article has been cited by other articles:
![]() |
J. A Belperio and A. Ardehali Chemokines and Transplant Vasculopathy Circ. Res., August 29, 2008; 103(5): 454 - 466. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. Niu, A. Azfer, O. Zhelyabovska, S. Fatma, and P. E. Kolattukudy Monocyte Chemotactic Protein (MCP)-1 Promotes Angiogenesis via a Novel Transcription Factor, MCP-1-induced Protein (MCPIP) J. Biol. Chem., May 23, 2008; 283(21): 14542 - 14551. [Abstract] [Full Text] [PDF] |
||||
![]() |
Q. Xu Stem Cells and Transplant Arteriosclerosis Circ. Res., May 9, 2008; 102(9): 1011 - 1024. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Chen, J. M. Abrahams, L. M. Smith, J. H. McVey, R. I. Lechler, and A. Dorling Regenerative repair after endoluminal injury in mice with specific antagonism of protease activated receptors on CD34+ vascular progenitors Blood, April 15, 2008; 111(8): 4155 - 4164. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. N. Mitchell and P. Libby Vascular Remodeling in Transplant Vasculopathy Circ. Res., April 13, 2007; 100(7): 967 - 978. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. F. Bentzon, C. Weile, C. S. Sondergaard, J. Hindkjaer, M. Kassem, and E. Falk Smooth Muscle Cells in Atherosclerosis Originate From the Local Vessel Wall and Not Circulating Progenitor Cells in ApoE Knockout Mice Arterioscler. Thromb. Vasc. Biol., December 1, 2006; 26(12): 2696 - 2702. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Jonas, J. C. Fang, J. C. Wang, S. Giri, D. Elian, Y. Har-Zahav, H. Ly, P. A. Seifert, J. J. Popma, and C. Rogers In-Stent Restenosis and Remote Coronary Lesion Progression Are Coupled in Cardiac Transplant Vasculopathy But Not in Native Coronary Artery Disease J. Am. Coll. Cardiol., August 1, 2006; 48(3): 453 - 461. [Abstract] [Full Text] [PDF] |
||||
![]() |
E. Minami, M. A. Laflamme, J. E. Saffitz, and C. E. Murry Extracardiac Progenitor Cells Repopulate Most Major Cell Types in the Transplanted Human Heart Circulation, November 8, 2005; 112(19): 2951 - 2958. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. Krebs, J. M. Tikkanen, A. I. Nykanen, J. Wood, M. Jeltsch, S. Yla-Herttuala, P. K. Koskinen, and K. B. Lemstrom Dual Role of Vascular Endothelial Growth Factor in Experimental Obliterative Bronchiolitis Am. J. Respir. Crit. Care Med., June 15, 2005; 171(12): 1421 - 1429. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Zhang, K. Peppel, L. Brian, L. Chien, and N. J. Freedman Vein Graft Neointimal Hyperplasia Is Exacerbated by Tumor Necrosis Factor Receptor-1 Signaling in Graft-Intrinsic Cells Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2277 - 2283. [Abstract] [Full Text] [PDF] |
||||
![]() |
N. Hattan, D. Warltier, W. Gu, C. Kolz, W. M. Chilian, and D. Weihrauch Autologous vascular smooth muscle cell-based myocardial gene therapy to induce coronary collateral growth Am J Physiol Heart Circ Physiol, August 1, 2004; 287(2): H488 - H493. [Abstract] [Full Text] [PDF] |
||||
![]() |
L. Zhang, N. J. Freedman, L. Brian, and K. Peppel Graft-Extrinsic Cells Predominate in Vein Graft Arterialization Arterioscler. Thromb. Vasc. Biol., March 1, 2004; 24(3): 470 - 476. [Abstract] [Full Text] |
||||
![]() |
Y. Hu, F. Davison, Z. Zhang, and Q. Xu Endothelial Replacement and Angiogenesis in Arteriosclerotic Lesions of Allografts Are Contributed by Circulating Progenitor Cells Circulation, December 23, 2003; 108(25): 3122 - 3127. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Hao, G. Gabbiani, and M.-L. Bochaton-Piallat Arterial Smooth Muscle Cell Heterogeneity: Implications for Atherosclerosis and Restenosis Development Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1510 - 1520. [Abstract] [Full Text] [PDF] |
||||
![]() |
G. Gabbiani and G. K. Hansson ATVB In Focus: Smooth Muscle Cells Arterioscler. Thromb. Vasc. Biol., March 1, 2003; 23(3): 379 - 379. [Full Text] [PDF] |
||||
|
ATVB Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |