CASP1 (Caspase 1)

Interleukin-18 (IL-18) is a pro-inflammatory cytokine, and higher IL-18 expression in pancreatic tumors is associated with poor prognosis. On the other hand, the release of active IL-18 was not observed with gemcitabine. These findings suggest that a low-nutrient tumor microenvironment and 5-FU therapy can promote caspase-8-dependent pyroptotic cell death with IL-18 activation, potentially contributing to chronic inflammation in pancreatic tumors.

Tumor cells undergoing disulfidptosis and pyroptosis elicit robust immune responses by promoting immune cell infiltration and reprogramming the immunosuppressive tumor microenvironment. This work presents a novel approach to induce disulfidptosis and pyroptosis through NADPH photo-oxidation and disruption of redox homeostasis, offering a promising strategy for the photocatalytic treatment of tumors.

NIEO exerts anti-RA effects by downregulating CASP1 and modulating the inflammasome pathway, validated through multi-omics and functional assays. The NE formulation overcomes bioavailability limitations, providing a framework for natural product-based drug discovery and positioning NIEO as a promising therapeutic candidate for RA.

The results show that KpEVs shape a liver microenvironment promoting gut-liver bacterial translocation, which may also influence HCC progression. Our study uncovers a previously unrecognized strategy by which K. pneumoniae exploits EVs to modulate host immunity of distant organs, highlighting tsRNAs as potential biomarkers and therapeutic targets.

These findings delineate the p75NTR extracellular domain-induced α-syn proteotoxic stress. This domain-specific mechanism advances our understanding of Parkinson's disease pathogenesis and highlights the therapeutic potential of targeting specific p75NTR domains.

Further, FF mix ameliorated hyperglycemia-induced angiogenesis (vascular endothelial growth factor, hypoxia-inducible factor 1α) and gliosis (glial fibrillary acidic protein) in the diabetic rats, accompanied by decreased inflammation (phosphorylated nuclear factor κB, tumor necrosis factor α, monocyte chemoattractant protein 1) and apoptosis (Bax, Bcl2, caspase3, and caspase12). This study illustrates the potential of an FF mix, attributed to the synergistic effects of its components, alleviating the progression of diabetic retinopathy by reducing diabetes-induced hypoxia, gliosis, and inflammation, while also inhibiting apoptosis in retinal cells.

This single-agent, tumor-specific initiation of pyroptosis, augmented by concomitant cuproptosis, elicits potent immunogenic cell death and robust systemic antitumor immunity, effectively suppressing primary and metastatic tumors while exhibiting a pristine safety profile. Our work establishes electron-shuttling coordination polymers as a versatile platform for developing safe and potent catalytic immunotherapies.

THJ alleviates angina symptoms and improves quality of life in SCAD patients, potentially through NLRP3 inflammasome inhibition and subsequent attenuation of pro-inflammatory cytokine release. These findings position THJ as a promising adjunct therapy for inflammation-driven coronary atherosclerosis. (Registration No. ChiCTR1900021772).

Furthermore, immunohistochemical analysis revealed increased CCL2 protein expression in the affected spinal cords. These findings suggest that systemic immune activation contributes to spinal neuroinflammation in DM, although its limited cellular infiltration implies a minor role in neurodegeneration.

Blocking IL-1R with Anakinra reduced IL1B expression, while inhibition of the P2X7 receptor with A740003 decreased NLRP3 and IL1B...Bioinformatics analysis of TCGA breast cancer samples showed differential inflammasome gene expression among subtypes and a positive correlation between inflammasome components and NET-related genes. These findings highlight the interplay between inflammatory and immune mechanisms in breast cancer progression and may support the development of new therapeutic strategies.

This review systematically clarifies its paradoxical roles by integrating caspase-1' s regulatory and context-dependent networks across PCD, epigenetics, tumor microenvironment, immune metabolism, and diverse diseases. Additionally, we summarize therapeutic progress and root causes of caspase-1 inhibitors' clinical failure as well as putting forward some innovative treatment strategies, aiming to offer new perspectives for future treating design.

These findings indicated that quercetin exerted a protective effect against ARHL by suppressing NLRP3 inflammasome activation and modulating mitophagy, providing a theoretical basis for applying quercetin to treat ARHL.