Apoptosis in cardiac transplant rejection

Leslie W. Miller, David J. Granville, Jagat Narula, Bruce M. McManus

Research output: Contribution to journalArticlepeer-review

29 Scopus citations

Abstract

Apoptosis occurs in human cardiac allograft rejection and may occur with all degrees of rejection and even in its absence. The prevalence and severity of apoptosis is determined predominantly by the intensity of macrophage infiltration and may be mediated by NO-related mechanisms. Apoptosis of interstitial, endothelial, and inflammatory cells is also present in heart allografts and may influence the degree and extent of vascular injury contributing to allograft rejection. Ongoing apoptosis of inflammatory cells suggests an immunoregulatory role. Studies of the involvement of NO in myocyte damage and Fas-FasL interactions in peripheral tolerance have raised the exciting possibility that these pathways can be exploited in a beneficial way. Further understanding of the role of apoptosis and the cellular and biochemical mechanisms that are involved in cardiac myocyte death and in inflammatory, endothelial, and interstitial cell death may provide insights into therapeutic modalities to suppress allograft rejection and vasculopathy.

Original languageEnglish (US)
Pages (from-to)141-154
Number of pages14
JournalCardiology Clinics
Volume19
Issue number1
DOIs
StatePublished - Jan 1 2001

Bibliographical note

Funding Information:
This work was supported in part by the St. Paul's Hospital Foundation and a grant-in-aid from the Heart and Stroke Foundation of British Columbia and Yukon (BMM).

Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.

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