Mitochondria‐derived damage‐associated molecular patterns and inflammation in the ischemic‐reperfused heart

Cardiac cell death after myocardial infarction release endogenous structures termed damage‐associated molecular patterns (DAMPs) that trigger the innate immune system and initiate a sterile inflammation in the myocardium. Cardiomyocytes are energy demanding cells and 30% of their volume are mitochon...

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Bibliographic Details
Published in:Acta Physiologica 2023-03, Vol.237 (3), p.e13920-n/a
Main Authors: Torp, May‐Kristin, Vaage, Jarle, Stensløkken, Kåre‐Olav
Format: Article
Language:English
Subjects:
cardiac cells
Cardiomyocytes
Cell death
Congestive heart failure
Endosymbionts
heart
Humans
Immune system
Immunogenicity
Inflammation
Inflammation - metabolism
Innate immunity
Ischemia
ischemia–reperfusion
Mitochondria
Mitochondria - metabolism
mitochondrial DAMPs
Myocardial infarction
Myocardial Infarction - metabolism
Myocardium
Myocardium - metabolism
Myocytes, Cardiac - metabolism
sterile inflammation
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Summary:Cardiac cell death after myocardial infarction release endogenous structures termed damage‐associated molecular patterns (DAMPs) that trigger the innate immune system and initiate a sterile inflammation in the myocardium. Cardiomyocytes are energy demanding cells and 30% of their volume are mitochondria. Mitochondria are evolutionary endosymbionts originating from bacteria containing molecular patterns similar to bacteria, termed mitochondrial DAMPs (mDAMPs). Consequently, mitochondrial debris may be particularly immunogenic and damaging. However, the role of mDAMPs in myocardial infarction is not clarified. Identifying the most harmful mDAMPs and inhibiting their early inflammatory signaling may reduce infarct size and the risk of developing post‐infarct heart failure. The focus of this review is the role of mDAMPs in the immediate pro‐inflammatory phase after myocardial infarction before arrival of immune cells in the myocardium. We discuss different mDAMPs, their role in physiology and present knowledge regarding their role in the inflammatory response of acute myocardial infarction.
ISSN:1748-1708
1748-1716
DOI:10.1111/apha.13920