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Inflammation Research
Erschienen in: Inflammation Research 9/2017

09.06.2017 | Review

Role of the immune system in cardiac tissue damage and repair following myocardial infarction

verfasst von: Arman Saparov, Vyacheslav Ogay, Talgat Nurgozhin, William C. W. Chen, Nurlan Mansurov, Assel Issabekova, Jamilya Zhakupova

Erschienen in: Inflammation Research | Ausgabe 9/2017

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Abstract

Introduction

The immune system plays a crucial role in the initiation, development, and resolution of inflammation following myocardial infarction (MI). The lack of oxygen and nutrients causes the death of cardiomyocytes and leads to the exposure of danger-associated molecular patterns that are recognized by the immune system to initiate inflammation.

Results

At the initial stage of post-MI inflammation, the immune system further damages cardiac tissue to clear cell debris. The excessive production of reactive oxygen species (ROS) by immune cells and the inability of the anti-oxidant system to neutralize ROS cause oxidative stress that further aggravates inflammation. On the other hand, the cells of both innate and adaptive immune system and their secreted factors are critically instrumental in the very dynamic and complex processes of regulating inflammation and mediating cardiac repair.

Conclusions

It is important to decipher the balance between detrimental and beneficial effects of the immune system in MI. This enables us to identify better therapeutic targets for reducing the infarct size, sustaining the cardiac function, and minimizing the likelihood of heart failure. This review discusses the role of both innate and adaptive immune systems in cardiac tissue damage and repair in experimental models of MI.
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Metadaten
Titel
Role of the immune system in cardiac tissue damage and repair following myocardial infarction
verfasst von
Arman Saparov
Vyacheslav Ogay
Talgat Nurgozhin
William C. W. Chen
Nurlan Mansurov
Assel Issabekova
Jamilya Zhakupova
Publikationsdatum
09.06.2017
Verlag
Springer International Publishing
Erschienen in
Inflammation Research / Ausgabe 9/2017
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI
https://doi.org/10.1007/s00011-017-1060-4

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