Does remote ischaemic conditioning reduce inflammation? A focus on innate immunity and cytokine response.
Basic Res Cardiol
; 116(1): 12, 2021 02 24.
Article
in English
| MEDLINE | ID: covidwho-1100964
ABSTRACT
The benefits of remote ischaemic conditioning (RIC) have been difficult to translate to humans, when considering traditional outcome measures, such as mortality and heart failure. This paper reviews the recent literature of the anti-inflammatory effects of RIC, with a particular focus on the innate immune response and cytokine inhibition. Given the current COVID-19 pandemic, the inflammatory hypothesis of cardiac protection is an attractive target on which to re-purpose such novel therapies. A PubMed/MEDLINE™ search was performed on July 13th 2020, for the key terms RIC, cytokines, the innate immune system and inflammation. Data suggest that RIC attenuates inflammation in animals by immune conditioning, cytokine inhibition, cell survival and the release of anti-inflammatory exosomes. It is proposed that RIC inhibits cytokine release via a reduction in nuclear factor kappa beta (NF-κB)-mediated NLRP3 inflammasome production. In vivo, RIC attenuates pro-inflammatory cytokine release in myocardial/cerebral infarction and LPS models of endotoxaemia. In the latter group, cytokine inhibition is associated with a profound survival benefit. Further clinical trials should establish whether the benefits of RIC in inflammation can be observed in humans. Moreover, we must consider whether uncomplicated MI and elective surgery are the most suitable clinical conditions in which to test this hypothesis.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Myocardial Reperfusion Injury
/
Cytokines
/
Ischemic Preconditioning, Myocardial
/
Immunity, Innate
/
Inflammation
Type of study:
Prognostic study
/
Reviews
Topics:
Long Covid
Limits:
Animals
/
Humans
Language:
English
Journal:
Basic Res Cardiol
Year:
2021
Document Type:
Article
Affiliation country:
S00395-021-00852-0
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