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Updated: Jul 17, 2025
An Intact Pericardium Ischemic Rodent Model
Published on: September 2, 2021
Association between NLRP3 inflammasome and periprocedural myocardial injury following elective PCI
Ao Chen1,2,3, Danbo Lu1,2,3, Zheng Yang1
1Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.
Background:
Periprocedural myocardial injury (PMI) is a common complication of percutaneous coronary intervention (PCI) associated with poor prognosis. Inflammation has been demonstrated to exert a crucial role in PMI. However, how the inflammation is initiated or sustained in PMI remains elusive.
Methods:
RNA-seq in peripheral blood mononuclear cells (PBMCs) from 3 Non-PMI and 6 PMI patients was performed with subsequent bioinformatics analysis. RNA-seq results were verified in a patient cohort. We also established the coronary microembolization (CME) mice model to mimic PMI. The activity of caspase-1 in PBMCs was detected by flow cytometry. The levels of interleukin (IL)-1β, IL-18 and cardiac troponin in plasma were measured by enzyme-linked immunosorbent assay.
Results:
We identified a total of 901 differentially expressed genes (DEGs) between Non-PMI and PMI patients. These DEGs participated in several inflammation-related processes. NOD-like receptor signaling pathway was significantly enriched in pathway analysis. All the key genes composed in the NLRP3 inflammasome, including NLRP3, PYCARD, CASP1 and IL1B, were upregulated in PMI patients. The activation of NLRP3 inflammasome was then verified by increased activity of caspase-1 in PBMCs, and elevated levels of IL-1β and IL-18 in plasma in PMI patients. Spearman analysis confirmed tight correlations between caspase-1 activity, IL-1β, IL-18 levels and troponin T level. In addition, caspase-1 activity, IL-1β and IL-18 levels were also enhanced in CME mice.
Conclusions:
We discovered that NLRP3 inflammasome was involved in PMI, thus providing evidence supporting the therapeutic value of NLRP3 inflammasome-targeted strategies in PMI.
Insights
Periprocedural myocardial injury (PMI) involves inflammation. Researchers found the NLRP3 inflammasome pathway is activated in PMI, suggesting it as a therapeutic target.
Area of Science:
- Cardiovascular Biology
- Immunology
- Molecular Medicine
Background:
- Periprocedural myocardial injury (PMI) following percutaneous coronary intervention (PCI) is a significant clinical issue.
- Inflammation plays a key role in PMI pathogenesis, but its initiation and perpetuation mechanisms remain unclear.
Purpose of the Study:
- To investigate the role of the NLRP3 inflammasome in periprocedural myocardial injury (PMI).
- To identify potential therapeutic targets for mitigating PMI.
Main Methods:
- RNA sequencing (RNA-seq) of peripheral blood mononuclear cells (PBMCs) from PMI and non-PMI patients.
- Bioinformatics analysis to identify differentially expressed genes (DEGs) and enriched pathways.
- Validation in a patient cohort and a coronary microembolization (CME) mouse model.
- Measurement of caspase-1 activity, IL-1β, IL-18, and troponin T levels.
Main Results:
- 901 DEGs were identified between PMI and non-PMI patients, enriched in inflammation-related pathways.
- Key components of the NLRP3 inflammasome (NLRP3, PYCARD, CASP1, IL1B) were upregulated in PMI patients.
- Increased caspase-1 activity and elevated IL-1β and IL-18 levels were observed in PMI patients and CME mice, correlating with troponin T levels.
Conclusions:
- The NLRP3 inflammasome is implicated in the pathogenesis of periprocedural myocardial injury (PMI).
- Targeting the NLRP3 inflammasome presents a promising therapeutic strategy for managing PMI.
