炎症体
酒精性肝病
嘌呤能受体
脂肪肝
酒精性肝炎
医学
肝病
肝损伤
化学
受体
脂肪性肝炎
病理生理学
目标2
细胞生物学
嘌呤能信号
炎症
半胱氨酸蛋白酶1
免疫学
疾病
上睑下垂
药理学
内科学
肝硬化
腺苷受体
兴奋剂
作者
Brendan Le Daré,Pierre-Jean Ferron,Thomas Gicquel
摘要
The World Health Organization has estimated that approximately 3 million deaths are attributable to alcohol consumption each year. Alcohol consumption is notably associated with the development and/or progression of many non-communicable inflammatory diseases—particularly in the liver. Although these alcoholic liver diseases were initially thought to be caused by the toxicity of ethanol on hepatocytes, the latest research indicates Kupffer cells (the liver macrophages) are at the heart of this “inflammatory shift”. Purinergic signaling (notably through P2X7 receptors and the NLRP3 inflammasome) by Kupffer cells appears to be a decisive factor in the pathophysiology of alcoholic liver disease. Hence, the modulation of purinergic signaling might represent a new means of treating alcoholic liver disease. Here, we review current knowledge on the pathophysiology of alcoholic liver diseases and therapeutic perspectives for targeting these inflammatory pathways.
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