<abstract xmlns="http://www.w3.org/1999/xhtml">

<p>Inflammation is involved in initiation, development and complications of the vast majority of non-communicable diseases. Recent research demonstrated that inflammation is involved in pathogenesis of all major cardiovascular diseases. Different endogenous factors (LDL, nucleic acid strands, uric acid – collectively called „Damage Associated Molecular Patterns – DAMPs”) activate dedicated receptors („Pattern Recognition Receptors – PRR”) on monocytes, macrophages or dendritic cells responsible for the innate immunologic response. They have a major role in natural defense mechanisms against different pathogens and in normal conditions have a protective role. Among PRRs „NOD-like, leucin rich, pyrin containing (NLRP)” receptors are a 14-member family located in the cytoplasm. One of these is the NLRP3 resulting from nuclear transcription under the influence of NF-kB, a second messenger from membrane PRRs to the nucleus. Mostly the same factors responsible for NLRP3 intracellular expression stimulate its oligomerization resulting in a large protein complex, the NLRP3 inflammasome. This activates caspase-1 responsible for IL-1b and IL-18 production and initiates an inflammatory reaction leading to various pathologic processes, such as atherosclerosis, hypertension, diabetes and heart failure. This is the current story as we know it of the NLRP3 inflammasome, a small intracellular component that when inappropriately activated may does more harm than good.</p>
</abstract>

Inflammation is involved in initiation, development and complications of the vast majority of non-communicable diseases. Recent research demonstrated that inflammation is involved in pathogenesis of all major cardiovascular diseases. Different endogenous factors (LDL, nucleic acid strands, uric acid – collectively called „Damage Associated Molecular Patterns – DAMPs”) activate dedicated receptors („Pattern Recognition Receptors – PRR”) on monocytes, macrophages or dendritic cells responsible for the innate immunologic response. They have a major role in natural defense mechanisms against different pathogens and in normal conditions have a protective role. Among PRRs „NOD-like, leucin rich, pyrin containing (NLRP)” receptors are a 14-member family located in the cytoplasm. One of these is the NLRP3 resulting from nuclear transcription under the influence of NF-kB, a second messenger from membrane PRRs to the nucleus. Mostly the same factors responsible for NLRP3 intracellular expression stimulate its oligomerization resulting in a large protein complex, the NLRP3 inflammasome. This activates caspase-1 responsible for IL-1b and IL-18 production and initiates an inflammatory reaction leading to various pathologic processes, such as atherosclerosis, hypertension, diabetes and heart failure. This is the current story as we know it of the NLRP3 inflammasome, a small intracellular component that when inappropriately activated may does more harm than good.

NLRP3 Inflammasome in Cardiovascular Disease: David's Stone against Goliath?

„Carol Davila” University of Medicine and Pharmacy

„Elias” Emergency University Hospital

Romanian Journal of Cardiology

This work is licensed under the Creative Commons Attribution 4.0 International License.

{"article-title":"NLRP3 Inflammasome in Cardiovascular Disease: David's Stone against Goliath?"}

Inflammation is involved in initiation, development and complications of the vast majority of non-communicable diseases. Recent research demonstrated that...

NLRP3 Inflammasome in Cardiovascular Disease: David's Stone against Goliath?

Article Category: Review

Published Online: May 05, 2022

Page range: 517 - 527

DOI: https://doi.org/10.47803/rjc.2021.31.3.517

Keywords
NLRP3 inflammasome, inflammation, outcome, CV disease

© 2021 Serban Balanescu et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

NLRP3 Inflammasome in Cardiovascular Disease: David's Stone against Goliath?

Article Category: Review

Published Online: May 05, 2022

Page range: 517 - 527

DOI: https://doi.org/10.47803/rjc.2021.31.3.517

KeywordsNLRP3 inflammasome, inflammation, outcome, CV disease

© 2021 Serban Balanescu et al., published by Sciendo

This work is licensed under the Creative Commons Attribution 4.0 International License.

Keywords
NLRP3 inflammasome, inflammation, outcome, CV disease