NLRP6 (NLR Family Pyrin Domain Containing 6)

A nephroprotective agent gastrodin was found to decrease NLRP6 and relieve mitochondria-mediated apoptosis caused by high fructose, possibly through promoting TRIM7-driven Bok mRNA degradation and FAM213A antioxidant effect. This study uncovered that high NLRP6 expression-driven mitochondria-mediated apoptosis could participate in podocyte injury and the suppression of NLRP6 by gastrodin may be an attractive therapeutic approach for podocyte injury.

We demonstrate that the E3 ligase UBE2O catalyzes dual-site monoubiquitination of NLRP6: at K680-687 to drive oligomerization via a conformational change, and at K115/130 within the nuclear localization signal to enforce cytoplasmic sequestration through steric hindrance. Furthermore, the UBE2O inhibitor arsenic trioxide suppresses NLRP6-dependent interleukin (IL)-18 secretion in acute promyelocytic leukemia (APL) patients. Thus, UBE2O-mediated dual-site monoubiquitination emerges as a central mechanism licensing NLRP6 inflammasome activation, revealing a new target for modulating intestinal immunity.

In this review, we present a comprehensive overview of inflammasomes with an emphasis on the mechanistic principles that govern inflammasome formation. We also discuss the contributions of inflammasome activation to health and disease.

Sivelestat sodium can improve lung function, correct PaO2/FiO2, and promote rehabilitation in patients with acute lung injury, which may be related to the regulation of NLRP6, ICAM-1, and other inflammatory factors.

Our findings highlight novel mutation loci that may explain the aggressive nature of XK ESCC. These insights could contribute to the development of early diagnostic and prognostic markers, as well as therapeutic targets, tailored for XK ESCC.

Besides, the upstream TF network of the 7 differentiated expressed pyroptosis-related key genes was constructed. Our team developed a diagnostic model for pyroptosis-related signatures in Alzheimer's disease, investigating ceRNA and TF regulatory networks, which may facilitate the diagnosis of AD with blood-based biomarkers.

NLRP6 promotes HCC progression by inhibiting macrophage infiltration and suppressing phagocytosis via the interaction between its PYD domain and E-Syt1's SMP domain. Transfer of Nlrp6 -/- macrophages is a promising therapeutic strategy for reducing HCC tumour growth.

Hypoxia, inflammation-related factors and the adipocyte secretome from patients with obesity upregulate mRNA levels of IL36G in HT-29 cancer cells. IL-36γ increase the gene expression levels of inflammation-related genes (IL36G, IL1A, IL1B, IL6, IL8 and NGAL) as well as ECM markers (MMP9, SPP1 and TNC) in HT-29 cells.

A nomogram including risk score and TNM stage demonstrated good prognostic ability in predicting 1-year, 3-year, and 5-year OS. We developed and verified a prognostic risk model based on PRGs for patients with HCC, which may provide a robust tool for predicting outcomes in this setting.

In this issue, Winsor and colleagues define a trans-kingdom interaction, which protects against colorectal cancer. Tritrichomonas protists initiate a Bacteroides bloom and sphingolipid release, which activates the NLRP6 inflammasome, enhancing protective mucus secretion by sentinel goblet cells.

Prophylactic administration of EA also significantly improved brain tissue damage, reduced neurological deficit score (P<0.01), cerebral infarction volume (P<0.01), inflammatory cell number (P<0.05), NLRP6, caspase-1, GSDMD-N mRNA and protein level (P<0.05 and P<0.01), ASC mRNA level and IL-1β protein level (P<0.01), and IL-1β and IL-18 level in brain tissue (P<0.01) compared to positive control. EA may serve as a potential drug for the treatment of brain I/R, which may exert an anti-inflammatory effect by inhibiting the activation of the inflammasome.