神经酰胺
鞘脂
疾病
生物
糖尿病
脂肪性肝炎
脂质代谢
营养感应
医学
生物信息学
内分泌学
脂肪肝
内科学
信号转导
细胞生物学
细胞凋亡
生物化学
作者
Joseph L. Wilkerson,Sean M. Tatum,William L. Holland,Scott A. Summers
标识
DOI:10.1152/physrev.00008.2023
摘要
Ceramides are signals of fatty acid excess that accumulate when a cell’s energetic needs have been met and its nutrient storage has reached capacity. As these sphingolipids accrue, they alter the metabolism and survival of cells throughout the body including in the heart, liver, blood vessels, skeletal muscle, brain, and kidney. These ceramide actions elicit the tissue dysfunction that underlies cardiometabolic diseases such as diabetes, coronary artery disease, metabolic-associated steatohepatitis, and heart failure. Here, we review the biosynthesis and degradation pathways that maintain ceramide levels in normal physiology and discuss how the loss of ceramide homeostasis drives cardiometabolic pathologies. We highlight signaling nodes that sense small changes in ceramides and in turn reprogram cellular metabolism and stimulate apoptosis. Finally, we evaluate the emerging therapeutic utility of these unique lipids as biomarkers that forecast disease risk and as targets of ceramide-lowering interventions that ameliorate disease.
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