OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
Liver injury and inflammation are the major factors triggering the development of metabolic dysfunction-associated steatotic liver disease (MASLD). Mechanisms for inflammation inhibition must exist to allow tissue resolution. Here, we use a novel knock-in mouse model to suppress Caspase-1 (CASP1) deactivation and thus prolong CASP1 activity. We fed mice a methionine-choline-deficient diet (MCD), to induce key features of MASLD, including inflammation, liver steatosis, and liver damage. Indeed, each of these features was elevated in Casp1.CDL mice compared to WT animals. Modelling a “lifestyle intervention”, we fed mice an MCD diet to induce MASLD and then switched to a healthier control diet, which resulted in liver recovery in WT mice, while Casp1.CDL mice had a delay in disease resolution. Our research findings address the important question of whether in vivo mechanisms for signal inhibition, such as self-limiting CASP1 activation, prevent disease progression in MASLD.
