Li Hongyao, Wu Ding, Zhang Haidan, Li Peiwu
Department of Emergency, Lanzhou University Second Hospital, Lanzhou University, Lanzhou, Gansu, 730030, China.
Heliyon. 2023 Jul 7;9(7):e18036. doi: 10.1016/j.heliyon.2023.e18036. eCollection 2023 Jul.
Acute pancreatitis (AP) may be associated with both local and systemic complications. Although it is usually self-limiting, up to 20% of patients develop severe acute pancreatitis (SAP), which leads to systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction and failure affecting the lung, kidney, liver and heart. Patients who survive the condition frequently develop devastating long-term consequences such as diabetes mellitus, exocrine pancreatic insufficiency, chronic pancreatitis (CP) and poor quality of life. A lack of specific targeted treatments is the main reason for high mortality and morbidity, indicating that more research on the pathogenesis of AP is needed. In the past decade, substantial advancements have been made in our understanding of the pathophysiological mechanisms of AP, including mechanisms of calcium-mediated acinar cell injury and death, the cytoprotective role of the unfolded protein response (UPR) and autophagy in preventing sustained endoplasmic reticulum stress (ERs); however, the mechanism of parenchymal cell death is relatively poorly understood. This paper reviews the research progress of the regulatory cell death (RCD) mode in the pathogenesis of AP, providing some new insights and regulatory targets for the pathogenesis and treatment of AP, facilitating better targeted drug development.
急性胰腺炎（AP）可能伴有局部和全身并发症。尽管它通常是自限性的，但高达20%的患者会发展为重症急性胰腺炎（SAP），进而导致全身炎症反应综合征（SIRS）以及影响肺、肾、肝和心脏的多器官功能障碍和衰竭。从这种疾病中存活下来的患者常常会出现诸如糖尿病、胰腺外分泌功能不全、慢性胰腺炎（CP）以及生活质量差等严重的长期后果。缺乏特异性靶向治疗是高死亡率和高发病率的主要原因，这表明需要对AP的发病机制进行更多研究。在过去十年中，我们对AP病理生理机制的理解取得了重大进展，包括钙介导的腺泡细胞损伤和死亡机制、未折叠蛋白反应（UPR）和自噬在预防持续性内质网应激（ERs）中的细胞保护作用；然而，实质细胞死亡的机制相对了解较少。本文综述了调节性细胞死亡（RCD）模式在AP发病机制中的研究进展，为AP的发病机制和治疗提供了一些新的见解和调节靶点，有助于更好地进行靶向药物开发。
