Page 56 - Read Online
P. 56
Feriozzi et al. Rare Dis Orphan Drugs J 2024;3:11 https://dx.doi.org/10.20517/rdodj.2023.37 Page 11 of 11
51. Jehn U, Bayraktar S, Pollmann S, et al. α-galactosidase a deficiency in Fabry disease leads to extensive dysregulated cellular signaling
pathways in human podocytes. Int J Mol Sci 2021;22:11339. DOI PubMed PMC
52. Braun F, Abed A, Sellung D, et al. Accumulation of α-synuclein mediates podocyte injury in Fabry nephropathy. J Clin Invest
2023;133:e157782. DOI PubMed
53. Germain DP. Reconceptualizing podocyte damage in Fabry disease: new findings identify α-synuclein as a putative therapeutic target.
Kidney Int 2024;105:237-9. DOI PubMed
54. Elsaid HOA, Furriol J, Blomqvist M, et al. Reduced α-galactosidase a activity in zebrafish (Danio rerio) mirrors distinct features of
Fabry nephropathy phenotype. Mol Genet Metab Rep 2022;31:100851. DOI PubMed PMC
