Abstract
Acute pancreatitis (AP) is an inflammatory disease of the pancreas that causes significant morbidity and mortality worldwide. Unfortunately, there is no specific treatment available to date. Several studies have previously shown that inhibitors of the PI3K/Akt axis downregulate the degree of inflammation in animal models of AP. However, studies on in vivo side-effects of such inhibitors are still lacking. In a recent issue of The Journal of Pathology, Chen, Malagola et al investigated if inhibition of Akt signaling plays a negative role in the regenerative phase of AP. They showed that treating AP mice with an Akt inhibitor (MK2206) impaired acinar regeneration and increased the development of acinar-to-ductal metaplasia. This is the first study to highlight the negative impact of an Akt inhibitor on cellular regeneration while simultaneously inhibiting inflammation in AP. The authors also suggested combining Akt activators to recover pancreatic regeneration. © 2020 The Authors. The Journal of Pathology published by John Wiley & Sons Ltd on behalf of Pathological Society of Great Britain and Ireland.
Highlights
Several studies have previously shown that inhibitors of the PI3K/Akt axis downregulate the degree of inflammation in animal models of Acute pancreatitis (AP)
They showed that treating AP mice with an Akt inhibitor (MK2206) impaired acinar regeneration and increased the development of acinar-to-ductal metaplasia
In the January 2020 issue of The Journal of Pathology, the study by Chen, Malagola et al [1] eloquently describes a potential mechanism of a therapeutic strategy to treat acute pancreatitis (AP) using a caerulein-induced injury model
Summary
Gallstones/biliary sludge and alcohol consumption are the most frequent causes of AP, whereas in animal (mostly rodent) models, AP is induced by various chemical or surgical strategies [4]. The most widely used mechanism is secretagogue hyper-stimulation induced by intraperitoneal injection of caerulein, as used in the study by Chen, Malagola et al [1]. This model does not require surgery or sophisticated manipulations, making it highly suitable for the investigation of intracellular signaling pathways. There is currently no definitive cure for AP, there are increasing reports in animal models that genetic ablation or pharmacological intervention of the PI3K–Akt
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