2018 Jul 7;19(7):1987 National Center for Biotechnology Information (2024)
We were able to include: (a) 42 DEPs, namely, angiotensin-converting enzyme 2 (ACE2), advanced glycosylation end-product specific receptor (AGER), agrin (AGRN), ALB, CCL2, CCL4, CCL11, CD3D, CD8A, CD19, CD38, CD69, HLA-DR, creatine phosphokinase (CKM), CLDN5, CSF2, CRP, CTNNB1, DKK1, ELANE, GPX1, hemoglobin A1 (HbA1), HP, HMGB1, interleukin-1 (IL-1), interleukin-1 (IL-1), IL-1RN (IL-1RA), IL-6, IL-10, LYZ, NFKB1 (NF-B), NOS2, OCLN, opioid receptor Kappa 1 (OPRK1), opioid receptor Mu 1 (OPRM1), proopiomelanocortin (POMC) as precursor of -endorphins, PTGS2, RSPO1, TLR4, TNF (TNF-), TNFRSF1A (TNFR60), and TNFRSF1B (TNFR80) and (b) 12 metabolic Kyoto Encyclopedia of Genes and Genomes (KEGG) 1 pathways, namely, C01290 (lactosylceramide), C02470 (xanthurenate), C10164 (picolinic acid), C03227 [3-OH-L-kynurenine (3OHK)], C11378 (coenzyme Q10), C00038 (zinc), C00070 (copper), C06428 [eicosapentaenoic acid (EPA)], C00027 [hydrogen peroxides (H 2 O 2 )], C19440 [malondialdehyde (MDA)], C004555 (DHEA), and C05926 (neopterin)
Further research is warranted to elucidate the full therapeutic potential of GLP-1 RAs in AS but like many genetic kidney diseases, Alport syndrome patients have been excluded from important clinical trials exploring therapeutics that slow the progression of CKD
Morad G, Helmink BA, Sharma P, Wargo JA
While they are highly effective for their intended purposes, they interact with various systems in the body
Indeed, previous reports indicate that GLP-1R signaling is blunted when dynamin-dependent endocytosis is inhibited chemically 10 or genetically 56
