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基于基因敲除技术综述AP腺泡细胞损伤的相关分子机制

The Molecular Mechanism of AP Acinar Cell Injury Based on Gene Knockout Technique
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摘要 急性胰腺炎(AP)是临床多发的危重消化系统疾病,胰腺腺泡细胞损伤是急性胰腺炎发生发展的重要病理机制之一。Ca^(2+)超载、氧化应激、自噬受损、内质网应激等途径被认为是胰腺腺泡细胞损伤的关键途径,但此过程中具体基因、蛋白和信号通路发挥作用的相关机制并不完全明确。基因敲除技术是揭示基因功能以及验证生物学信号转导途径最有效的方法,为进一步明确急性胰腺炎胰腺腺泡细胞损伤的分子机制提供了新的技术手段。该文基于基因敲除技术系统综述了AP腺泡细胞损伤的相关分子机制,以期进一步明确急性胰腺炎腺泡细胞损伤相关病理生理机制,促进临床特效药物开发,提高急性胰腺炎临床疗效并改善患者预后。 AP(acute pancreatitis)is a clinically multiple critical digestive system disease.Pancreatic acinar cell injury is one of the important pathological mechanisms of the occurrence and development of acute pancreatitis.Ca^(2+)overload,oxidative stress,autophagy damage,endoplasmic reticulum stress and other pathways are considered to be the key pathways of pancreatic acinar cell injury.However,the related mechanisms of specific genes,proteins and signaling pathways in this process are not completely clear.Gene knockout technology is the most effective method to reveal gene function and verify biological signal transduction pathway,which provides a new technical means to further clarify the molecular mechanism of pancreatic acinar cell injury in acute pancreatitis.This paper systematically reviewed the molecular mechanisms of acinar cell injury in AP based on gene knockout technology,in order to further clarify the pathophysiology of acinar cell injury in acute pancreatitis,promote the development of specific clinical drugs,improve the clinical efficacy of acute pancreatitis and improve the prognosis of patients.
作者 王琼 汪湛东 宋冰 白敏 汪永锋 张延英 文林林 赵泓彰 杨润泽 WANG Qiong;WANG Zhandong;SONG Bing;BAI Min;WANG Yongfeng;ZHANG Yanying;WEN Linlin;ZHAO Hongzhang;YANG Runze(School of Basic Medicine,Gansu University of Traditional Chinese Medicine,Lanzhou 730000,China;Gansu Experimental Animal Industry Technology Center,Lanzhou 730000,China)
出处 《中国细胞生物学学报》 CAS CSCD 2023年第1期75-83,共9页 Chinese Journal of Cell Biology
基金 国家自然科学基金(批准号:82160871) 甘肃省自然科学基金(批准号:22JR5RA591、20JR5RA186) 甘肃省中医药管理局重点项目(批准号:GZKZ-2021-10)资助的课题。
关键词 急性胰腺炎 基因敲除 Ca^(2+)超载 氧化应激 自噬受损 内质网应激 acute pancreatitis gene knockout Ca^(2+)overload oxidative stress impaired autophagy ER stress
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