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Treatment options to break the cycle of recurrent pericarditis.
Curr Opin Cardiol
January 2025
Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota, USA.
Purpose Of Review: This review provides a contemporary, evidence-based update on the pathophysiological mechanisms and rapidly evolving therapeutic options for recurrent pericarditis.
Recent Findings: Recent studies have elucidated the pathogenesis of recurrent pericarditis, identifying autoinflammation as a key mechanism and interleukin-1 (IL-1) as a central modulator of the inflammatory cascade. Multiple clinical trials have investigated novel therapeutic approaches, particularly focusing on IL-1 inhibition.
Dysregulation of the NLRP3 Inflammasome and Promotion of Disease by IL-1β in a Murine Model of Sandhoff Disease.
Cells
January 2025
Department of Pharmacology, University of Oxford, Mansfield Road, Oxford OX1 3QT, UK.
Sandhoff disease (SD) is a progressive neurodegenerative lysosomal storage disorder characterized by GM2 ganglioside accumulation as a result of mutations in the gene, which encodes the β-subunit of the enzyme β-hexosaminidase. Lysosomal storage of GM2 triggers inflammation in the CNS and periphery. The NLRP3 inflammasome is an important coordinator of pro-inflammatory responses, and we have investigated its regulation in murine SD.
View Article and Find Full Text PDFIL-1 blockade in myocardial infarction and its efficacy in patients with complex coronary artery disease. Another brick in the wall.
J Cardiovasc Pharmacol
January 2025
School of Cardiovascular and Metabolic Medicine & Sciences, King's College London British Heart Foundation Centre of Excellence, James Black Centre, 125 Coldharbour Lane, London, SE5 9NU, UK.
SOX2-induced IL1α-mediated immune suppression drives epithelial dysplasia malignant transformation.
bioRxiv
December 2024
Department of Head and Neck Surgery, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Squamous cell carcinomas (SCC) are often preceded by potentially malignant precursor lesions, most of which remain benign. The terminal exhaustion phenotypes of effector T-cells and the accumulation of myeloid-derived suppressor cells (MDSC) have been thoroughly characterized in established SCC. However, it is unclear what precancerous lesions harbor a bona fide high risk for malignant transformation and how precancerous epithelial dysplasia drives the immune system to the point of no return.
View Article and Find Full Text PDFNLRP3 Inflammasome Upregulates PD-L1 in Ovarian Cancer and Contributes to an Immunosuppressive Microenvironment.
Immunotargets Ther
December 2024
Department of Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150081, People's Republic of China.
Introduction: The NLRP3 inflammasome has been implicated in the initiation of inflammation and tumorigenesis; however, its role in epithelial ovarian cancer (EOC) remains unclear.
Methods: This study employed high-throughput sequencing data, ELISA, clone formation assay, Western blot, and flow cytometric analysis to investigate the specific role of the NLRP3 inflammasome in EOC.
Results: NLRP3 was highly expressed in human EOC tissues and correlated with an unfavorable prognosis.
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