Gorelick Fred S, Lerch Markus M
Yale University Medical School and Veterans Affairs Medical Center, West Haven, Connecticut.
Department of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Cell Mol Gastroenterol Hepatol. 2017 Jun 10;4(2):251-262. doi: 10.1016/j.jcmgh.2017.05.007. eCollection 2017 Sep.
Acute pancreatitis is currently the most common cause of hospital admission among all nonmalignant gastrointestinal diseases. To understand the pathophysiology of the disease and as a potential step toward developing targeted therapies, attempts to induce the disease experimentally began more than 100 years ago. Recent decades have seen progress in developing new experimental pancreatitis models as well as elucidating many underlying cell biological and pathophysiological disease mechanisms. Some models have been developed to reflect specific causes of acute pancreatitis in human beings. However, the paucity of data relating to the molecular mechanisms of human disease, the likelihood that multiple genetic and environmental factors affect the risk of disease development and its severity, and the limited information regarding the natural history of disease in human beings make it difficult to evaluate the value of disease models. Here, we provide an overview of key models and discuss our views on their strengths for characterizing cell biological disease mechanisms or for identifying potential therapeutic targets. We also acknowledge their limitations.
急性胰腺炎是目前所有非恶性胃肠疾病中最常见的住院原因。为了了解该疾病的病理生理学,并作为开发靶向治疗的潜在步骤,100多年前就开始尝试通过实验诱导该疾病。近几十年来,在开发新的实验性胰腺炎模型以及阐明许多潜在的细胞生物学和病理生理学疾病机制方面取得了进展。已经开发了一些模型来反映人类急性胰腺炎的特定病因。然而,与人类疾病分子机制相关的数据匮乏、多种遗传和环境因素影响疾病发生风险及其严重程度的可能性,以及关于人类疾病自然史的信息有限,使得难以评估疾病模型的价值。在此,我们概述了关键模型,并讨论了我们对它们在表征细胞生物学疾病机制或识别潜在治疗靶点方面的优势的看法。我们也承认它们的局限性。