DPP4 valorphin activate NR4As pathway and OPA1 that protect from CoQ10 deficiency from OPA1 dysfunctions and from WMH
DOI:
https://doi.org/10.47363/JJCMR/2023(3)160Keywords:
Hemorphin (valorphin), Chronic Cerebral Hypoperfusion, Oxidative Stress, Inflammation , White Matter Hyperintensity, Glucocorticoid-Beta, B-arrestins , B-Adrenergic, Oxytocin, Nrf2 , Ang2-AT2 , VEGF-A , Microglia , Astrocytes , Primary coenzyme CoQ10,01110 mTORC1, S6K , tyrosine , Thr , Leu , Île , Val , Glu/Gln , Gly , Ser , tryptophan , Arginine, Plasma glial fibrillary acidic protein (GFAP), IL6 , IL17 , T-cells , Mitochondrial OPA1 disorders , Severe Traumatic Brain , Mineralocorticoid , WMH Tissue with high cations binding , Tissue with proper anions binding , Cellular tissue of CoQ10 deficiency contains high cations binding, GTPase , ATPase , Dopamine , Serotonin , MelatoninAbstract
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.
Opioid receptors produce powerful analgesia that is effective in participating in the function of the immune cells, and effective for modulating acquired immune responses (include modulating lymphocytes functions). While tryptophan (and both leucine and Tyr kinases) is necessary to activate both serotonin and lymphocytes functions, that the reduction in tryptophan, in Tyr, and in Leu will be result in decreasing in serotonin and in Nrf2 followed by reduction in platelets production, reduction in lymphocytes functions and reductions in hematopoietic cells functions that will be result of cerebral small vessel disease, and white matter hyperintensity.
Serotonin (5-hydroxytryptamine; 5-HT) is a growth factor for hematopoietic cells promote the megakaryocytes (MKs) proliferation which produces platelets, where reduction in serotonin will be result of decreasing in megakaryocytes proliferation followed by reduction in hematopoiesis which associated with white matter microstructure.