炎症是导致全球数百万人患病的罪魁祸首。大量研究揭示了炎症和炎性介质如细胞因子和趋化因子与各种蛋白质的表达和活性改变有关，特别是药物代谢酶如细胞色素P450酶（CYPs）。大多数可用的报道都是强调炎症导致CYPs下调，随后其底物浓度增加，并与炎性介质如白细胞介素6和肿瘤坏死因子-alpha之间的联系。然而，报道也表明炎症影响着与药物受体相互作用的其他蛋白质的表达和/或活性。这些多方面的参与使得炎症的临床后果出人意料。这些变化在许多炎症性疾病中都得到了证实，包括类风湿性关节炎、克罗恩病、急性呼吸道疾病以及自然老化等。例如，一些常用的心血管药物在患有类风湿性关节炎和克罗恩病等炎症性疾病时失去了其疗效。有趣的是，这是尽管浓度增加却随后减少。这种观察结果归结于目标受体蛋白如钙和钾通道和β-肾上腺素受体以及代谢酶的表达同时减少。本综述总结了当前对炎症对CYPs和药物受体靶蛋白的影响的理解和临床意义。 © 2023年Abdallah，Chahal，Jamali和Mahmoud的版权所有。

Inflammation is a culprit in many conditions affecting millions of people worldwide. A plethora of studies has revealed that inflammation and inflammatory mediators such as cytokines and chemokines are associated with altered expression and activity of various proteins such as those involved in drug metabolism, specifically cytochrome P450 enzymes (CYPs). Emphasis of most available reports is on the inflammation-induced downregulation of CYPs, subsequently an increase in their substrate concentrations, and the link between the condition and the inflammatory mediators such as interleukin-6 and tumor necrosis factor alpha. However, reports also suggest that inflammation influences expression and/or activity of other proteins such as those involved in the drug-receptor interaction. These multifaced involvements render the clinical consequence of the inflammation unexpected. Such changes are shown in many inflammatory conditions including rheumatoid arthritis, Crohn's disease, acute respiratory illnesses as well as natural processes such as aging, among others. For example, some commonly used cardiovascular drugs lose their efficacy when patients get afflicted with inflammatory conditions such as rheumatoid arthritis and Crohn's disease. Interestingly, this is despite increased concentration subsequent to reduced clearance. The observation is attributed to a simultaneous reduction in the expression of target receptor proteins such as the calcium and potassium channel and β-adrenergic receptor as well as the metabolic enzymes. This narrative review summarizes the current understanding and clinical implications of the inflammatory effects on both CYPs and drug-receptor target proteins.Copyright © 2023 Abdallah, Chahal, Jamali and Mahmoud.