Publications by authors named "S Kirschnek"
Article Synopsis
- Mitochondria play complex roles in two different cell death pathways: apoptosis and pyroptosis, particularly regarding NLRP3 inflammasome activation, but their exact mechanisms are not well understood.
- The study found that activating NLRP3 while inhibiting apoptosis occurs when cells are under stress from various stimuli like nigericin and viruses, as these activators affect mitochondrial function rather than just triggering inflammasome activation.
- NLRP3 activation needs a combination of signals—one from disrupted mitochondrial processes and another from specific NLRP3 activators—suggesting that both oxidative phosphorylation inhibition and apoptosis suppression influence cell fate.
Myeloid cells are the first line of defence against pathogens. Mitochondrial apoptosis signalling is a crucial regulator of myeloid cell lifespan and modulates the function of myeloid cells. The anti-apoptotic protein BCL-2-family protein BCL2A1/A1/BFL-1 is strongly upregulated in inflammation in macrophages.
View Article and Find Full Text PDFArticle Synopsis
- - Mitochondria respond to infections with signals that can trigger inflammation, but the full understanding of how this works is still being explored.
- - The study reveals that the enzyme caspase-activated DNase (CAD) plays a key role in activating mitochondrial pro-inflammatory responses, aiding the body's defense against viral infections.
- - In experiments, cells and mice lacking CAD showed weakened immune responses to viral infections, indicating that CAD is crucial for linking mitochondrial activity to inflammation and overall immune defense.
Paracetamol (acetaminophen, APAP) overdose severely damages mitochondria and triggers several apoptotic processes in hepatocytes, but the final outcome is fulminant necrotic cell death, resulting in acute liver failure and mortality. Here, we studied this switch of cell death modes and demonstrate a non-canonical role of the apoptosis-regulating BCL-2 homolog BIM/Bcl2l11 in promoting necrosis by regulating cellular bioenergetics. BIM deficiency enhanced total ATP production and shifted the bioenergetic profile towards glycolysis, resulting in persistent protection from APAP-induced liver injury.
View Article and Find Full Text PDF