title: Necroptosis: a potential, promising target and switch in acute pancreatitis.
abstract: Pancreatic acinar cell death is the major pathophysiological change in early acute pancreatitis (AP), and the death modalities are important factors determining its progression and prognosis. During AP, acinar cells undergo two major modes of death, including necrosis and apoptosis. Acinar 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. Necroptosis is a newly discovered cell death modality characterized by both necrosis and apoptosis, i.e., it is actively regulated by special genes, while has the typical morphological features of necrosis. Currently, necroptosis is gradually becoming an important topic in the fields of inflammatory diseases. The preliminary results from necroptosis in AP have confirmed the existence of acinar cell necroptosis, which may be a potential target for effectively regulating inflammatory injuries and improving its outcomes; however, the functional changes and mechanisms of necroptosis still require further investigation. This article reviewed the progress of necroptosis in AP to provide a reference for deeply understanding the pathogenic mechanisms of AP and identifying new therapeutic targets.
authors.affiliation: Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
authors.forename: Gang
authors.initials: G
authors.lastname: Wang
authors.affiliation: Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
authors.forename: Feng-Zhi
authors.initials: FZ
authors.lastname: Qu
authors.affiliation: Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
authors.forename: Le
authors.initials: L
authors.lastname: Li
authors.affiliation: Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China.
authors.forename: Jia-Chen
authors.initials: JC
authors.lastname: Lv
authors.affiliation: Department of Pancreatic and Biliary Surgery, The First Affiliated Hospital of Harbin Medical University, 23 Youzheng Street, Nangang District, Harbin, 150001, Heilongjiang, China. sunbei70@tom.com.
authors.forename: Bei
authors.initials: B
authors.lastname: Sun
mesh_terms: D061354:Acinar Cells / Q000502:physiology; D000818:Animals; D017209:Apoptosis; D006801:Humans; D058847:Inflammasomes / Q000502:physiology; D058990:Molecular Targeted Therapy; D009336:Necrosis; D010179:Pancreas / Q000473:pathology*; D019283:Pancreatitis, Acute Necrotizing / Q000188:drug therapy / Q000473:pathology*; D015398:Signal Transduction
chemical_list: D058847:Inflammasomes
keywords: Acute pancreatitis; Damage-associated molecular patterns; Endoplasmic reticulum stress; Inflammasome; Necroptosis