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

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

Research output: Contribution to journalReview articlepeer-review

17 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)739-751
Number of pages13
JournalInflammation Research
Issue number9
Publication statusPublished - Sep 2017
Externally publishedYes


  • Journal Article
  • Review

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