PTB Seminar ptb.univie.ac.at #WeckwerthLab in der Konrad-Lorenz Villa in Altenberg. Wir sitzen im ehemaligen Arbeitszimmer von Konrad Lorenz und diskutieren Themen der Wissenschafts - und Gesellschaftsethik.
CONGRATULATIONS: New publication by Wan Li from #WeckwerthLab: Hesperitin, a natural product from citrus fruits, protects against non-alcoholic fatty liver disease (NAFLD), a major cause for metabolic syndrome, diabetes and cardiovascular diseases. pubs.acs.org/doi/10.1021/...
new publication about natural variation of biological nitrification inhibition in a wheat germplasm collection. #rootexudatemetabolomics
onlinelibrary.wiley.com/doi/10.1111/...
medienportal.univie.ac.at/en/media/rec...
new publication about the holobiont concept for sustainable agroecosystems www.cell.com/trends/plant...
www.nature.com/articles/s41...
Clusia species exhibit diverse photosynthetic physiotypes. The authors present genome assemblies for C. major (weak CAM), C. minor s.l. (facultative CAM), and C. rosea (strong CAM), and speculate that...
Focus on the interaction between the microbiome and plants
medienportal.univie.ac.at
Palmitic acid-induced lipotoxicity contributes to the development of nonalcoholic fatty liver disease (NAFLD). Hesperetin has been reported to alleviate oxidative stress, inflammation, and cell death in NAFLD, while its potential to mitigate palmitic acid-induced lipotoxicity remains unexplored. This study investigates the protective effects of hesperetin on palmitic-acid-stimulated lipotoxicity and elucidates the underlying molecular mechanisms. Our results showed that hesperetin decreased palmitic acid-activated lipotoxicity through inhibition of the intrinsic apoptosis pathway and promotion of autophagic flux. Metabolomics analysis and stable-isotope-tracing data indicated that hesperetin treatment restored the aberrant tricarboxylic acid cycle caused by palmitic acid exposure, accompanied by a decrease in anaplerotic flux from glutamine to α-ketoglutarate. The reduction of α-ketoglutarate resulted in the inhibition of mTORC1 signaling, which in turn activated autophagy and limited apoptosis. Furthermore, hesperetin activated AMPK, which coordinated with mTORC1 to regulate autophagy. Additionally, hesperetin reinstated the activation of AKT and Nrf2, further protecting the cell against the deleterious effects of lipotoxicity. These data highlight the role of glutaminolysis as a survival mechanism for preventing lipotoxicity upon hesperetin treatment.
Plant evolution is largely driven by plant–microbe interactions, yet the ecology of
the plant holobiont is not well understood at a molecular level. However, these relationships
hold diverse benefits ...
