NLRP3 Inflammasome in Acute Myocardial Infarction

Mauro, Adolfo G; Bonaventura, Aldo; Mezzaroma, Eleonora; Quader, Mohammed; Toldo, Stefano

doi:10.1097/fjc.0000000000000717

Cited by 82 publications

(71 citation statements)

References 151 publications

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“…The common, final stage of this process is the proteolytic cleavage of pro-IL-1β and pro-IL-18 to their active forms. The NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome was largely studied in the CV field, as confirmed by their role in atherosclerosis, acute myocardial infarction, heart failure, and pericarditis [71][72][73][74][75][76]. Of note, the role of the NLRP3 inflammasome and IL-1β is well established in many rheumatic diseases, too [77].…”

Section: Nets and The Inflammasomementioning

confidence: 99%

“…Actually, we now know that the NLRP3 inflammasome activation is important in the determination of the infarct size (mainly through pyroptosis) [96,97] and in the so-called "wavefront of reperfusion injury," through which the infarct size expands in the 3-6 h after reperfusion through an increasing activation of the NLRP3 inflammasome [94]. For a more in-depth discussion on the role of the NLRP3 inflammasome, readers are referred elsewhere [13,75,95]. Therefore, the link between NETs and the NLRP3 inflammasome in the pathophysiology of AMI is still under investigation and not completely understood yet.…”

Section: Nets and The Inflammasomementioning

confidence: 99%

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Neutrophil Extracellular Traps and Cardiovascular Diseases: An Update

Bonaventura

Vecchiè

Abbate

et al. 2020

Cells

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121

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Neutrophil extracellular traps (NETs) are formed by decondensed chromatin, histones, and neutrophil granular proteins and have a role in entrapping microbial pathogens. NETs, however, have pro-thrombotic properties by stimulating fibrin deposition, and increased NET levels correlate with larger infarct size and predict major adverse cardiovascular (CV) events. NETs have been involved also in the pathogenesis of diabetes, as high glucose levels were found to induce NETosis. Accordingly, NETs have been described as drivers of diabetic complications, such as diabetic wound and diabetic retinopathy. Inflammasomes are macromolecular structures involved in the release of pro-inflammatory mediators, such as interleukin-1, which is a key mediator in CV diseases. A crosstalk between the inflammasome and NETs is known for some rheumatologic diseases, while this link is still under investigation and not completely understood in CV diseases. In this review, we summarized the most recent updates about the role of NETs in acute myocardial infarction and metabolic diseases and provided an overview on the relationship between NET and inflammasome activities in rheumatologic diseases, speculating a possible link between these two entities also in CV diseases.

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Section: Nets and The Inflammasomementioning

confidence: 99%

Section: Nets and The Inflammasomementioning

confidence: 99%

Neutrophil Extracellular Traps and Cardiovascular Diseases: An Update

Bonaventura

Vecchiè

Abbate

et al. 2020

Cells

Self Cite

121

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“…In addition to TGFB, inflammation has been directly involved in the suppression of cardiac autophagy with age. The Nucleotide-Binding Oligomerization Domain, Leucine Rich Repeat and Pyrin Domain Containing 3 (NLRP3) inflammasome initiates an inflammatory form of cell death that has been implicated in cardiac disease [76][77][78]. NLRP3-deficient (NLRP3 −/− ) mice display longer lifespans, preserved cardiac function, and reduced fibrosis when compared to age-matched littermate controls.…”

Section: Autophagy Suppression In Cardiac Agingmentioning

confidence: 99%

Protein and Mitochondria Quality Control Mechanisms and Cardiac Aging

Ghosh

Vinod

Symons

et al. 2020

Cells

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Cardiovascular disease (CVD) is the number one cause of death in the United States. Advancing age is a primary risk factor for developing CVD. Estimates indicate that 20% of the US population will be ≥65 years old by 2030. Direct expenditures for treating CVD in the older population combined with indirect costs, secondary to lost wages, are predicted to reach $1.1 trillion by 2035. Therefore, there is an eminent need to discover novel therapeutic targets and identify new interventions to delay, lessen the severity, or prevent cardiovascular complications associated with advanced age. Protein and organelle quality control pathways including autophagy/lysosomal and the ubiquitin-proteasome systems, are emerging contributors of age-associated myocardial dysfunction. In general, two findings have sparked this interest. First, strong evidence indicates that cardiac protein degradation pathways are altered in the heart with aging. Second, it is well accepted that damaged and misfolded protein aggregates and dysfunctional mitochondria accumulate in the heart with age. In this review, we will: (i) define the different protein and mitochondria quality control mechanisms in the heart; (ii) provide evidence that each quality control pathway becomes dysfunctional during cardiac aging; and (iii) discuss current advances in targeting these pathways to maintain cardiac function with age.

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“…NLR consists of three domains, with leucine-rich repeats (LRR) at the C-terminal, responsible for the identification and binding of specific PAMP and DAMP [16]. Nucleotide-binding oligomerization domain (NOD) in the middle is the characteristic of NLR, also known as the NACHT domain, named by the first letter of four known NLR family members [17].…”

Section: Structure Of Nlrp3mentioning

confidence: 99%

NLRP3 Inflammasome: A Potential Alternative Therapy Target for Atherosclerosis

Yang

Yin

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Atherosclerosis (AS) is a complex and chronic inflammatory disease that occurs in multiple systems of the human body. It is an important pathological basis for a variety of diseases and a serious threat to human health. So far, many theories have been formed to explain the pathogenesis of atherosclerosis, among which “inflammation theory” has gradually become a research focus. This theory presents that inflammatory response runs through the whole progress of AS, inflammatory cells play as the main executors of AS, and inflammatory mediators are the key molecules of AS. In the inflammatory process of atherosclerosis, the role of NLRP3 in the atherosclerosis has gradually got the attention of researchers. NLRP3 is a kind of signal-transductional pattern recognition receptors (PRRs). After recognizing and binding to the damage factors, NLRP3 inflammasome will be assembled to activate IL-1β and caspase-1 pathways, resulting in promoting the inflammation process of AS, reducing the stability of the plaques, and finally increasing the incidence of adverse cardiovascular events. Taken above, the article will review the potential benefits of drugs targeting the NLRP3 inflammasome in the therapy of AS.

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NLRP3 Inflammasome in Acute Myocardial Infarction

Cited by 82 publications

References 151 publications

Neutrophil Extracellular Traps and Cardiovascular Diseases: An Update

Neutrophil Extracellular Traps and Cardiovascular Diseases: An Update

Protein and Mitochondria Quality Control Mechanisms and Cardiac Aging

NLRP3 Inflammasome: A Potential Alternative Therapy Target for Atherosclerosis

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