Enzyme imbalance disrupts pancreas-to-insulin cell signaling

Researchers identified how excess pancreatic elastase breaks communication between insulin-producing cells and their neighboring tissues, potentially explaining dysfunction in diabetes and pancreatic disease. The discovery targets a specific cellular mechanism that could lead to new therapeutic interventions for conditions affecting millions globally.

Originaltitel: Excess pancreatic elastase alters acinar-β cell communication by impairing the mechano-signaling and the PAR2 pathways