Recent insights into the cellular mechanisms of acute pancreatitis
- PMID: 17225878
- PMCID: PMC2656626
- DOI: 10.1155/2007/930424
Recent insights into the cellular mechanisms of acute pancreatitis
Abstract
In acute pancreatitis, initiating cellular events causing acinar cell injury includes co-localization of zymogens with lysosomal hydrolases, leading to premature enzyme activation and pathological exocytosis of zymogens into the interstitial space. This is followed by processes that accentuate cell injury; triggering acute inflammatory mediators, intensifying oxidative stress, compromising the microcirculation and activating a neurogenic feedback. Such localized events then progress to a systemic inflammatory response leading to multiorgan dysfunction syndrome with resulting high morbidity and mortality. The present review discusses some of the most recent insights into each of these cellular processes postulated to cause or propagate the process of acute pancreatitis, and also the role of alcohol and genetics.
En cas de pancréatite aiguë, l’initiation d’événements cellulaires causant des lésions cellulaires acineuses inclut la colocalisation de proenzymes avec des hydrolases lysosomiales entraînant une activation enzymatique prématurée et une exocytose pathologique des proenzymes dans l’espace interstitiel. Ces phénomènes sont suivis de processus qui accentuent la lésion cellulaire, déclenchant des médiateurs inflammatoires aigus, intensifiant le stress oxydatif, compromettant la microcirculation et activant les rétroactions neurogènes. Ces événements localisés évoluent ensuite vers une rétroaction inflammatoire systémique provoquant un syndrome de dysfonctionnement multiviscéral entraînant un taux de morbidité et de mortalité élevé. La présente analyse expose certains des aperçus les plus récents sur chacun de ces processus cellulaires qu’on pense causer ou propager le processus de pancréatite aigu, et également le rôle de l’alcool et de la génétique.
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