Next Article in Journal
Aquaporins in Urinary Extracellular Vesicles (Exosomes)
Next Article in Special Issue
T-Tubular Electrical Defects Contribute to Blunted β-Adrenergic Response in Heart Failure
Previous Article in Journal
Genome-Wide Discriminatory Information Patterns of Cytosine DNA Methylation
Previous Article in Special Issue
The Protective Role of the TOPK/PBK Pathway in Myocardial Ischemia/Reperfusion and H2O2-Induced Injury in H9C2 Cardiomyocytes
Article Menu
Issue 6 (June) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2016, 17(6), 958; doi:10.3390/ijms17060958

Targeting the Innate Immune Response to Improve Cardiac Graft Recovery after Heart Transplantation: Implications for the Donation after Cardiac Death

1
VCU Pauley Heart Center and Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA
2
Department of Cardiothoracic Surgery, Virginia Commonwealth University, Richmond, VA 23298, USA
3
VCU Johnson Research Center, Virginia Commonwealth University, Richmond, VA 23298, USA
4
Department of Pharmacotherapy and Outcome Sciences, Virginia Commonwealth University, Richmond, VA 23298, USA
*
Author to whom correspondence should be addressed.
Academic Editor: H. W. M. Niessen
Received: 5 April 2016 / Revised: 30 May 2016 / Accepted: 1 June 2016 / Published: 17 June 2016
(This article belongs to the Special Issue Improvement of Cardiac Function in Heart Failure 2017)
View Full-Text   |   Download PDF [2193 KB, uploaded 17 June 2016]   |  

Abstract

Heart transplantation (HTx) is the ultimate treatment for end-stage heart failure. The number of patients on waiting lists for heart transplants, however, is much higher than the number of available organs. The shortage of donor hearts is a serious concern since the population affected by heart failure is constantly increasing. Furthermore, the long-term success of HTx poses some challenges despite the improvement in the management of the short-term complications and in the methods to limit graft rejection. Myocardial injury occurs during transplantation. Injury initiated in the donor as result of brain or cardiac death is exacerbated by organ procurement and storage, and is ultimately amplified by reperfusion injury at the time of transplantation. The innate immune system is a mechanism of first-line defense against pathogens and cell injury. Innate immunity is activated during myocardial injury and produces deleterious effects on the heart structure and function. Here, we briefly discuss the role of the innate immunity in the initiation of myocardial injury, with particular focus on the Toll-like receptors and inflammasome, and how to potentially expand the donor population by targeting the innate immune response. View Full-Text
Keywords: heart transplantation; graft failure; rejection; donation after brain death (DBD); donation after cardiac death (DCD); inflammasome; Toll-like receptors; innate immune response; ischemia-reperfusion injury heart transplantation; graft failure; rejection; donation after brain death (DBD); donation after cardiac death (DCD); inflammasome; Toll-like receptors; innate immune response; ischemia-reperfusion injury
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Toldo, S.; Quader, M.; Salloum, F.N.; Mezzaroma, E.; Abbate, A. Targeting the Innate Immune Response to Improve Cardiac Graft Recovery after Heart Transplantation: Implications for the Donation after Cardiac Death. Int. J. Mol. Sci. 2016, 17, 958.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top