Our network approaches identified 51 SnGs highly conserved across the human tissues, including CDKN1A ( p21 )-centered regulators that control cell cycle progression and the senescence-associated secretory phenotype (SASP). Through a comprehensive transcriptomic network analysis of 50 human tissues in the Genotype-Tissue Expression Project (GTEx) cohort, we identified SnG-enriched gene modules, characterized SnG co-expression patterns, and constructed aggregated SnG networks across primary tissues of the human body. This study performed an integrative gene network analysis of bulk and single-cell RNA-seq data in non-diseased human tissues to investigate SnG co-expression signatures and their cell-type specificity. However, the prevalence of senescent cells in healthy human tissues and the global SnG expression signature in different cell types are poorly understood. Enormous efforts have been made to identify and characterize senescence genes (SnGs) in stress and disease systems. Multiple developmental and environmental factors, such as intrinsic cellular cues, radiation, oxidative stress, oncogenes, and protein accumulation, activate genes and pathways that can lead to senescence. Taken together, these data suggest that the clinical spectrum from benign to overt clinical autoimmunity may partially result from or trigger a complex interplay among specific microbial profiles, anti-Ro autoantibodies, and genetics.Ĭellular senescence is a complex stress response that impacts cellular function and organismal health. In addition to documenting differences in microbial relative abundances across clinical severity of disease, these data provide a first-time demonstration that microbial differences are correlated with HLA SLE-risk alleles. Four genera exhibited evidence of an interaction with anti-Ro52 IgA: Lachnoclostridium, Romboutsia, Bacteroides and Actinomyces (P <. Multiple genera within the families Ruminococcaceae and Lachnospiraceae showed evidence of an HLA-by-genus interaction (P <. Those taxa that showed differential relative abundances were then tested for whether the effect size differed depending on the women's HLA SLE-risk allele genotype (DRB1*03:01, DRB1*15:01, DQB1*02:01 and DQB1*06:02) or anti-SSA/Ro autoantibody levels. Differences in microbial relative abundances among these three groups were tested assuming an ordering in clinical severity (HC ![]() The most common muscular dystrophies are Duchenne muscular dystrophy, myotonic dystrophy types 1 and 2, and facioscapulohumeral dystrophy. Muscular dystrophies are a heterogeneous group of inherited progressive disorders of muscle characterized pathologically by destruction of muscle and its replacement by fatty and fibrous tissue.
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