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FXS results from loss of function of the fragile X mental retardation 1 ( FMR1 ) gene, which encodes the fragile X mental retardation protein (FMRP), a RNA-binding protein important for the regulation of local dendritic protein translation (Bagni and Greenough 2005

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This dysbiotic transformation precipitates compromised SCFA biosynthetic capacity, disruption of intestinal epithelial barrier integrity, and the pathological phenomenon of intestinal hyperpermeability or “leaky gut syndrome.” The consequent translocation of gut-derived pathogen-associated molecular patterns (PAMPs), exemplified by lipopolysaccharides, orchestrates chronic low-grade inflammation through Toll-like receptor (TLR) activation and cascading pro-inflammatory cytokine release, thereby accelerating epithelial-mesenchymal transition within renal tubular epithelium and promoting progressive interstitial fibrogenesis (Rukavina Mikusic et al., 2020