title: Central role of mitochondrial injury in the pathogenesis of acute pancreatitis.
abstract: Acute pancreatitis is an inflammatory disease with no specific treatment. One of the main reasons behind the lack of specific therapy is that the pathogenesis of acute pancreatitis is poorly understood. During the development of acute pancreatitis, the disease-inducing factors can damage both cell types of the exocrine pancreas, namely the acinar and ductal cells. Because damage of either of the cell types can contribute to the inflammation, it is crucial to find common intracellular mechanisms that can be targeted by pharmacological therapies. Despite the many differences, recent studies revealed that the most common factors that induce pancreatitis cause mitochondrial damage with the consequent breakdown of bioenergetics, that is, ATP depletion in both cell types. In this review, we summarize our knowledge of mitochondrial function and damage within both pancreatic acinar and ductal cells. We also suggest that colloidal ATP delivery systems for pancreatic energy supply may be able to protect acinar and ductal cells from cellular damage in the early phase of the disease. An effective energy delivery system combined with the prevention of further mitochondrial damage may, for the first time, open up the possibility of pharmacological therapy for acute pancreatitis, leading to reduced disease severity and mortality.
authors.affiliation: First Department of Medicine, University of Szeged, Szeged, Hungary.
authors.forename: J
authors.initials: J
authors.lastname: Maléth
authors.forename: Z
authors.initials: Z
authors.lastname: Rakonczay
authors.forename: V
authors.initials: V
authors.lastname: Venglovecz
authors.forename: N J
authors.initials: NJ
authors.lastname: Dolman
authors.forename: P
authors.initials: P
authors.lastname: Hegyi
mesh_terms: D000818:Animals; D006801:Humans; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology*; D010195:Pancreatitis / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology*