Abstract

Pancreatic acinar cell death is the major pathophysiological change in early acute pancreatitis (AP), which is important factor determining its progression and prognosis. During AP, acinar cell death is composed of necrosis and apoptosis. Acinar cell necrosis can lead to intensely local and systemic inflammatory responses, which both induce and aggravate the lesion. Necrosis has long been considered an unregulated and passive cell death process. Since the effective interventions of necrosis are difficult to perform, its relevant studies have not received adequate attention. Programmed cell necrosis is a newly discovered cell death characterized by both necrosis and apoptosis, it is actively regulated by special genes, while has the typical morphological features of necrosis. Programmed cell necrosis which may be a potential target for the preliminary results in AP have confirmed the existence of acinar cell effectively regulating inflammatory injuries and improving its outcomes, however, the functional changes and mechanisms of programmed cell necrosis still require further investigation. This article reviews the progress of programmed cell necrosis in AP to provide a reference for deeply understanding the pathogenic mechanisms of AP and identifying new therapeutic targets. Key words: Acute Pancreatitis; Programmed cell necrosis; Damage-associated molecular patterns; Apoptosis; Autophagy

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