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caspase-1

Mechanism of miR-378a-3p Enriched in M2 Macrophage-Derived Extracellular Vesicles in Cardiomyocyte Pyroptosis after MI

[Hypertension Research] An in vitro cell model was established, followed by a comprehensive evaluation of cell viability and pyroptosis. The binding relationships of miR-378a-3p and ELAVL1, HuR, and NLR family pyrin domain containing 3 were analyzed.

NLRP3 Inflammasome Activation in Human Peripheral Blood Mononuclear Cells Induced by Venoms Secreted PLAM2s

[International Journal of Biological Macromolecules] Peripheral blood mononuclear cells were isolated by density gradient and incubated with RPMI, LPS, BthTX-I or BthTX-II isolated from Bothrops jararacussu venom, to evaluate viability, and the results showed that there was no cell death.

SARS-CoV-2 Targets the Lysosome to Mediate Airway Inflammatory Cell Death

[Autophagy] Emerging evidence suggests that SARS-CoV-2 could trigger pyroptosis, a form of inflammatory programmed cell death characterized by the activation of inflammasomes and caspase 1 and the formation of transmembrane pores by gasdermin D.

Downregulating Expression of OPTN Elevates Neuroinflammation via AIM2 Inflammasome- and RIPK1-Activating Mechanisms in APP/PS1 Transgenic Mice

[Journal of Neuroinflammation] Neuroinflammation is thought to be a cause of Alzheimer’s disease (AD), which is partly caused by inadequate mitophagy. As a receptor of mitophagy, the authors revealed the regulatory roles of optineurin (OPTN) on neuroinflammation in the pathogenesis of AD.

Luxeptinib Disables NLRP3 Inflammasome-Mediated IL-1β Release and Pathways Required for Secretion of Inflammatory Cytokines IL-6 and TNFα

[Biochemical Pharmacology] Luxeptinib inhibited the release of three cytokines from THP-1 monocytes and macrophages at concentrations of 0.1 µM and above.

ASC Speck Formation after Inflammasome Activation in Primary Human Keratinocytes

[Oxidative Medicine and Cellular Longevity] Scientists showed that UVB provoked apoptosis-associated speck-like protein (ASC) speck formation in human primary keratinocytes prior to cell death, and that specks were, opposed to the perinuclear cytosolic localization in myeloid cells, formed in the nucleus.

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