Targeting a key protein reduces injury in steatotic liver transplantation

Background and aims

Steatotic donor livers are highly susceptible to post-transplant dysfunction; however, the underlying mechanisms remain incompletely understood. This study aimed to investigate the role of galectin-3 (LGALS3)-mediated pyroptosis in steatotic liver graft injury and explore its therapeutic potential.

Methods

Results

Conclusions

This study systematically demonstrated that LGALS3 promotes inflammasome activation and pyroptosis after steatotic liver transplantation by regulating the ubiquitination of NLRP3, thereby exacerbating graft injury. Targeted inhibition of LGALS3 and its downstream NLRP3 signaling axis significantly improved liver function and survival outcomes in steatotic liver transplantation models. These findings not only expand our understanding of the molecular mechanisms underlying complications in steatotic liver transplantation but also provide a theoretical and experimental basis for developing novel anti-pyroptotic therapies, with substantial scientific and clinical implications for liver transplantation and other I/R-associated liver diseases.

Source:

Xia & He Publishing Inc.

Journal reference: