CREBH regulation of lipid metabolism through multifaceted functions that improve arteriosclerosis.

CREBH regulation of lipid metabolism through multifaceted functions that improve arteriosclerosis.
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CREBH通过改善动脉硬化的多方面功能调节脂质代谢。

DOI:
10.1111/jdi.13766
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发表时间:
2022-07
影响因子:
3.2
通讯作者:
--
中科院分区:
医学3区
文献类型:
--
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环腺苷单磷酸反应元件结合蛋白H (CREBH)通过调节载脂蛋白激活脂蛋白脂肪酶(LPL)活性。活化的LPL水解富含甘油三酯的脂蛋白,如极低密度脂蛋白(VLDL)和乳糜微粒,产生残余脂蛋白。CREBH增加载脂蛋白E (ApoE),这是一种介导残余颗粒清除的配体,并减少干扰残余颗粒清除的apo3。CREBH还可以改善介导残体清除的VLDL受体(VLDLR)和LDL受体相关蛋白1 (LRP1)蛋白。因此,CREBH促进血液中残留颗粒的清除,减少动脉粥样硬化斑块面积。CREBH诱导成纤维细胞生长因子21 (FGF21)分泌到血液中,降低血浆甘油三酯。CREBH产生ApoA1,从而增加血浆HDL -胆固醇水平。
Cyclic adenosine monophosphate‐responsive element‐binding protein H (CREBH) activates lipoprotein lipase (LPL) activity by modulating apolipoproteins. Activated LPL hydrolyzes triglyceride‐rich lipoproteins, such as very low‐density lipoprotein (VLDL) and chylomicrons, resulting in remnant lipoproteins. CREBH increases apolipoprotein E (ApoE), a ligand that mediates the clearance of remnant particles and reduces ApoC3, which interferes with remnant clearance. CREBH also improves VLDL receptor (VLDLR) and LDL receptor‐related protein 1 (LRP1) protein that mediates remnant clearance. Therefore, CREBH promotes the clearance of remnant particles from the blood, decreasing the atherogenic plaque area. CREBH induces the secretion of fibroblast growth factor 21 (FGF21) into the blood, decreasing plasma triglyceride. CREBH produces ApoA1 and so increases plasma HDL‐cholesterol levels.
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