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 article

5 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)739-751
Number of pages13
JournalInflammation Research
Volume66
Issue number9
DOIs
Publication statusPublished - Sep 2017
Externally publishedYes

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Immune System
Myocardial Infarction
Inflammation
Reactive Oxygen Species
Likelihood Functions
Cardiac Myocytes
Oxidants
Cause of Death
Oxidative Stress
Theoretical Models
Heart Failure
Oxygen
Food
Therapeutics

Keywords

  • Journal Article
  • Review

Cite this

Saparov, A., Ogay, V., Nurgozhin, T., Chen, W. C. W., Mansurov, N., Issabekova, A., & Zhakupova, J. (2017). Role of the immune system in cardiac tissue damage and repair following myocardial infarction. Inflammation Research, 66(9), 739-751. https://doi.org/10.1007/s00011-017-1060-4

Role of the immune system in cardiac tissue damage and repair following myocardial infarction. / Saparov, Arman; Ogay, Vyacheslav; Nurgozhin, Talgat; Chen, William C W; Mansurov, Nurlan; Issabekova, Assel; Zhakupova, Jamilya.

In: Inflammation Research, Vol. 66, No. 9, 09.2017, p. 739-751.

Research output: Contribution to journalReview article

Saparov, A, Ogay, V, Nurgozhin, T, Chen, WCW, Mansurov, N, Issabekova, A & Zhakupova, J 2017, 'Role of the immune system in cardiac tissue damage and repair following myocardial infarction', Inflammation Research, vol. 66, no. 9, pp. 739-751. https://doi.org/10.1007/s00011-017-1060-4
Saparov, Arman ; Ogay, Vyacheslav ; Nurgozhin, Talgat ; Chen, William C W ; Mansurov, Nurlan ; Issabekova, Assel ; Zhakupova, Jamilya. / Role of the immune system in cardiac tissue damage and repair following myocardial infarction. In: Inflammation Research. 2017 ; Vol. 66, No. 9. pp. 739-751.
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AU - Saparov, Arman

AU - Ogay, Vyacheslav

AU - Nurgozhin, Talgat

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AU - Mansurov, Nurlan

AU - Issabekova, Assel

AU - Zhakupova, Jamilya

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N2 - 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.

AB - 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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