ArticleScientific reports2024
Acute exposure to LPS induces cardiac dysfunction via the activation of the NLRP3 inflammasome.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Ferroptosis-related gene EPAS1 suppresses breast cancer progression by inhibiting M2 macrophage polarization.Discover oncology · 2026Article
- Evaluation of immunoglobulin A1/immunoglobulin A2 ratio and B cell lymphoma-6 in relation to apoptosis-associated speck-like protein in diabetic kidney disease patients.BMC immunology · 2026Article
- Advances in the mechanisms of the NLRP3 inflammasome in sepsis‑induced cardiomyopathy and targeted therapeutic studies (Review).Molecular medicine reports · 2026Review
- Bacteroides coprocola protects dopaminergic neurons in rotenone-induced Parkinson's disease mouse model by modulating gut microbiota dysbiosis and inhibiting the NLRP3 signaling pathway.Translational neurodegeneration · 2026Article
- A Novel Role for the Small Molecule Cinnamaldehyde in Protecting AgainstAntioxidants (Basel, Switzerland) · 2026Article
- Elevated Serum LPS in Newly Diagnosed Hashimoto's Thyroiditis: A Case-Control Study in Bulgaria.Clinics and practice · 2026Article
- Cellular and Molecular Mechanisms Explaining the Link Between Inflammatory Bowel Disease and Heart Failure.Cells · 2025Review
- The role of gut microbiota dysbiosis in the inflammatory pathogenesis of diabetic retinopathy.Frontiers in immunology · 2025Review
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Authors and funding
5 authors.
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Abstract
Systemic inflammation contributes to left ventricular (LV) dysfunction, however the role of the NLRP3 inflammasome in LV dysfunction in acute inflammatory conditions is unclear. This study investigated the role of the NLRP3 inflammasome in acute (24 h) cardiac structural and functional changes in vivo and in vitro in lipopolysaccharide (LPS)-induced inflammation. LPS-treated Sprague-Dawley (SD) rats showed increased LPS metabolite abundance in their LVs as measured by atmospheric pressure matrix-assisted laser desorption ionisation (AP-MALDI) mass spectrometry imaging (MSI). Echocardiography and histology showed that in LPS-exposed rats, LV internal diameter was decreased, with evidence of macrophage infiltration and oedema. However, there were no changes in LV wall thickness or collagen volume. Additionally, LPS-exposed rats exhibited impaired LV relaxation, potentially contributing to decreased stroke volume. While global systolic function was preserved, LPS exposure in SD rats resulted in impaired myocardial deformation assessed by speckle-tracking echocardiography. Exposure to LPS resulted in upregulation of the expression of components of the NLRP3 inflammasome in rodents. In vitro LPS exposure resulted in increased gene expression of NLRP3 and downstream cytokines IL-1β and IL-18, antioxidant SOD2, and elevated markers of pyroptosis (GSDMD) which were inhibited by treatment with a NLRP3 antagonist. However, LPS-induced increases in the gene expression of apoptosic markers (BAX/Bcl2) were not impacted by NLRP3 antagonism. These findings suggest that inflammation induced adverse cardiac structural and functional changes is, at least in part, mediated by the NLRP3 inflammasome in acute, high-grade inflammatory states. In addition, in vitro findings suggest that while the NLRP3 inflammasome mediates pyroptotic pathways, regulation of apoptosis that is independent of the inflammasome.
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