Chinetti G, Fruchart J C, Staels B
U.325 TNSERM, Département d'Athérosclerose, Institut Pasteur de Lille, France.
Inflamm Res. 2000 Oct;49(10):497-505. doi: 10.1007/s000110050622.
Peroxisome proliferator-activated (PPARs) are ligand-activated transcription factors belonging to the nuclear receptor family. PPARs function as regulators of lipid and lipoprotein metabolism and glucose homeostasis and influence cellular proliferation, differentiation and apoptosis. PPARalpha is highly expressed in tissues such as liver, muscle, kidney and heart, where it stimulates the beta-oxidative degradation of fatty acids. PPARgamma is predominantly expressed in intestine and adipose tissue. PPARgamma triggers adipocyte differentiation and promotes lipid storage. The hypolipidemic fibrates and the antidiabetic glitazones are synthetic ligands for PPARalpha and PPARgamma, respectively. Furthermore, fatty acids and eicosanoids are natural PPAR ligands: PPARalpha is activated by leukotriene B4, whereas prostaglandin J2 is a PPARgamma ligand. These observations suggested a potential role for PPARs not only in metabolic but also in inflammation control. The first evidence for a role of PPARalpha in inflammation control came from the demonstration that PPARalpha deficient mice display a prolonged response to inflammatory stimuli. It was suggested that PPARalpha deficiency results in a reduced beta-oxidative degradation of these inflammatory fatty acid derivatives. More recently, PPAR activators were shown to inhibit the activation of inflammatory response genes (such as IL-2, IL-6, IL-8, TNFalpha and metalloproteases) by negatively interfering with the NF- kappaB, STAT and AP-1 signalling pathways. PPAR activators exert these anti-inflammatory activities in different immunological and vascular wall cell types such as monocyte/macrophages, endothelial, epithelial and smooth muscle cells in which PPARs are expressed. These recent findings indicate a modulatory role for PPARs in the control of the inflammatory response with potential therapeutic applications in inflammation-related diseases, such as atherosclerosis and inflammatory bowel disease.
过氧化物酶体增殖物激活受体(PPARs)是属于核受体家族的配体激活转录因子。PPARs作为脂质和脂蛋白代谢以及葡萄糖稳态的调节因子,影响细胞增殖、分化和凋亡。PPARα在肝脏、肌肉、肾脏和心脏等组织中高度表达,在这些组织中它刺激脂肪酸的β氧化降解。PPARγ主要在肠道和脂肪组织中表达。PPARγ触发脂肪细胞分化并促进脂质储存。降血脂的贝特类药物和抗糖尿病的格列酮类药物分别是PPARα和PPARγ的合成配体。此外,脂肪酸和类花生酸是天然的PPAR配体:PPARα被白三烯B4激活,而前列腺素J2是PPARγ的配体。这些观察结果表明PPARs不仅在代谢中而且在炎症控制中都具有潜在作用。PPARα在炎症控制中发挥作用的首个证据来自于PPARα缺陷小鼠对炎症刺激表现出延长反应的证明。有人提出PPARα缺陷导致这些炎症性脂肪酸衍生物的β氧化降解减少。最近,PPAR激活剂被证明通过负向干扰NF-κB、STAT和AP-1信号通路来抑制炎症反应基因(如IL-2、IL-6、IL-8、TNFα和金属蛋白酶)的激活。PPAR激活剂在不同的免疫和血管壁细胞类型(如单核细胞/巨噬细胞、内皮细胞、上皮细胞和平滑肌细胞,这些细胞中表达PPARs)中发挥这些抗炎活性。这些最新发现表明PPARs在炎症反应控制中具有调节作用,在动脉粥样硬化和炎症性肠病等炎症相关疾病中具有潜在的治疗应用。