In this study, we show that Atg7 induces excessive autophagy activation in the INS-1(823/13) cell line exposed to PA and that Atg7-induced CTSB overexpression contributes to an NLRP3-dependent proinflammatory response and subsequently impairs GSIS independently of apoptosis.

Oct 18, 2013 · Silencing of Nod-like receptor 3 (NLRP3) completely abolished both IL-1β secretion and the down-regulation effects of Atg7-induced CTSB overexpression on glucose-stimulated insulin secretion impairment, thus identifying the NLRP3 inflammasome as an autophagy-responsive element in the pancreatic INS-1(823/13) cell line.

May 5, 2020 · Genetic analyses using ATG7-deficient cells indicate that neutrophils secrete IL-1β via an autophagy-dependent mechanism. These findings reveal fundamental differences in GSDMD trafficking...

Here, we explore the intracellular machinery that maintains skin homeostasis by suppressing UVB-induced inflammasome activation in human keratinocytes. We found that pharmacological inhibition of autophagy promoted UVB-induced NLRP3 inflammasome activation.

Silencing of Nod-like receptor 3 (NLRP3) completely abolished both IL-1 secretion and the down-regu-lation effects of Atg7-induced CTSB overexpression on glucose-stimulated insulin secretion impairment, thus identifying the NLRP3 inflammasome as an autophagy-responsive element in the pancreatic INS-1(823/13) cell line.

Our study establishes a novel pathophysiological role for CM NLRP3-inflammasome signaling with a mechanistic link to the pathogenesis of AF, and establishes inhibition of NLRP3 as a potential novel AF-therapy approach.

In this review, we systematically summarized the current understanding of the activation mechanism of NLRP3 inflammasome, and the pathological changes in AS involving NLRP3. We also discussed potential therapeutic strategies targeting NLRP3 inflammasome to combat AS.

Dec 14, 2023 · Mitochondria, lysosomes, the Golgi apparatus, and other organelles all have important roles in NLRP3 inflammasome activation. NLRP3 inflammasome activation triggers caspase 1 activation, which cleaves pro-IL-1β, pro-IL-18, and gasdermin D (GSDMD) to produce their active forms.

Jul 30, 2024 · We found that UVB radiation induces ATG5/ATG7-independent alternative (noncanonical) autophagy, which leads to suppression of NLRP3 inflammasome activation through the clearance of damaged mitochondria in UVB-irradiated keratinocytes.

Jul 22, 2014 · Here we demonstrate a novel role for autophagy in the clearance of extracellular Aβ fibrils by microglia and in the regulation of the Aβ-induced NLRP3 (NLR family, pyrin domain containing 3) inflammasome using microglia specific atg7 knockout mice and cell cultures.