作者: D. Zepeda-Orozco , M. Kong , R.H. Scheuermann
DOI: 10.1016/J.TRANSPROCEED.2015.04.086
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摘要: Abstract Background In kidney transplantation (KT), progression of chronic histological damage with subclinical inflammation is associated poor long-term allograft survival. The role nonimmunological pathways in injury has not been fully assessed. Methods We analyzed a public microarray dataset that used 1-year protocol transplant biopsy specimens to investigate whether genes and might influence outcome. selected included 3 patient/sample groups based on their findings: normal histology (n = 25), interstitial fibrosis alone (IF alone, n = 24), (IF+i, 16). IF+i group had lower death-censored graft survival renal function patients mean follow-up 4 years. performed statistical analysis comparing gene expression patterns the samples. Results Gene cluster enrichment group-specific demonstrated divergent pattern between mitochondrial immune response genes, downregulation group. ontological downregulated identified generation precursor metabolite energy, oxidative stress as most significant biological processes. transcription regulation pathway factors involved biogenesis. Conclusions molecular signature dysfunction reflects energetic insufficiency, inadequate antioxidant mitochondria biogenesis worse Thus, impairment appears be an important nonimmune factor injury.