DPP4 valorphin 可激活 NR4As 通路和 OPA1,从而防止因 CoQ10 缺乏而导致的 OPA1 功能障碍和 WMH

A. Tantawi
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摘要

瓦洛啡(又称 VV-hemorphin-5 )是九种必需氨基酸:Leu_Val_Val_Tyr、_Pro _Pro _Thr_ Gln_& Arg 在激活线粒体功能以及激活促进催产素和 Nrf2 合成的血清素和 NR4As 途径方面发挥重要作用。由于 mTORC1 和 S6K 基因及亚基的极化性增加,Thr、Tph (TGG)、Glu、Gln (cycle) 和亮氨酸的缺乏会导致 OPA1 修复紊乱或缺乏,这可能是原发性辅酶 Q10(CoQ10)缺乏症的结果,该病的特点是线粒体内膜受损,而线粒体内膜是激活糖皮质激素受体 GCR 合成所必需的。线粒体损伤或失调会导致促炎因子的积累,从而引起亚基和蛋白质的突变。色氨酸、甘氨酸(被认为是色氨酸三联体的镜像)和氩氨酸的减少会导致脯氨酸合成减少,进而导致 tRNA 减少,继而导致线粒体 OPA1 修复和功能减少(甘氨酸的减少会导致 GTPase 减少)、IL17 合成减少,促炎分子积累,血清素合成减少,所有 GC-beta、oxitocin 和 Nrf2 生成减少,巨核细胞增殖减少,造血减少,导致白质密度增高。
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DPP4 valorphin activate NR4As pathway and OPA1 that protect from CoQ10 deficiency from OPA1 dysfunctions and from WMH
Valorphin (known as VV-hemorphin-5 ) is nine essential amino acids : Leu_Val_Val_Tyr, _Pro _Pro _Thr_ Gln_& Arg are having important role in activating mitochondrial functions and in activating both serotonin and NR4As pathway that promote oxytocin and Nrf2 synthesis. Deficiency in Thr, Tph (TGG), Glu, Gln (cycle) and Leucine due to increasing in the polarizability in mTORC1 and in S6K genes and subunits can cause disorders or deficiency in OPA1 repair that can be the result of Primary coenzyme Q10 (CoQ10) deficiency disease that characterized by damage in the inner mitochondrial membrane which is necessary for activating glucocorticoids receptor GCR Synthesis. Mitochondrial damage or disorder can lead to accumulation in pro-inflammation which can cause mutations in subunit and protein. The reduction in tryptophan, in Gly (which considered as the mirror of tryptophan triplets), and in Arg will cause reductions in Proline synthesis and consequently reductions in tRNAs, followed by reduction in mitochondrial OPA1 repairs and functions (that reduction in Gly can cause reduction in GTPase), followed by reduction in IL17 synthesis and accumulation of proinflammatory molecules, and followed by reduction in serotonin synthesis and in all of GC-beta, oxitocin, and Nrf2 production, that will be followed by decreasing in megakaryocytes proliferation and followed by reduction in hematopoiesis which associated to white matter hyperintensity
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