<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE289nnn/GSE289932/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Homo sapiens</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE289932</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Anti-inflammatory and phosphorylation effects of CFTR modulator triple therapy in cystic fibrosis</name><description>Cystic Fibrosis is an autosomal recessive disorder caused by mutations in the CFTR gene, which encodes a key chloride channel, leading to impaired ion transport and severe progressive respiratory failure. CFTR modulators, such as Trikafta© has improved morbidity in CF, but its systemic effects remain unclear. This study evaluated the clinical outcomes, safety, and cellular mechanisms of Trikafta© in young children (&lt; 11 years) with CF using a multi-omic approach. Seventeen children with CF (median age 8.7 years, 26% female) and 12 healthy controls (median age 9.6 years, 42% female) were included for multi-omic analysis. The analysis included RNA sequencing, proteomics and phosphoproteomics. Baseline pathway enrichment analysis (FDR &lt; 0.05) revealed systemic inflammation, transmembrane transporter deficiencies, reduced protein kinase, and reduced GTPase activity. Three months post-Trikafta© treatment, anti-inflammatory effects, epigenetic modulation, and increased protein kinase activity were observed, indicating partial reversal of cellular abnormalities. Trikafta© improves clinical outcomes and reduces inflammation, epigenetic changes and key phosphorylation pathways in young children with CF, offering insights into CF pathology and potential biomarkers for monitoring treatment.</description><dates><publication>2026/08/03</publication></dates><accession>GSE289932</accession><cross_references><GSM>GSM8801794</GSM><GSM>GSM8801795</GSM><GSM>GSM8801796</GSM><GSM>GSM8801830</GSM><GSM>GSM8801797</GSM><GSM>GSM8801831</GSM><GSM>GSM8801798</GSM><GSM>GSM8801810</GSM><GSM>GSM8801799</GSM><GSM>GSM8801832</GSM><GSM>GSM8801811</GSM><GSM>GSM8801833</GSM><GSM>GSM8801834</GSM><GSM>GSM8801812</GSM><GSM>GSM8801813</GSM><GSM>GSM8801814</GSM><GSM>GSM8801815</GSM><GSM>GSM8801816</GSM><GSM>GSM8801817</GSM><GSM>GSM8801818</GSM><GSM>GSM8801819</GSM><GSM>GSM8801791</GSM><GSM>GSM8801792</GSM><GSM>GSM8801793</GSM><GSM>GSM8801820</GSM><GSM>GSM8801821</GSM><GSM>GSM8801822</GSM><GSM>GSM8801800</GSM><GSM>GSM8801823</GSM><GSM>GSM8801801</GSM><GSM>GSM8801802</GSM><GSM>GSM8801824</GSM><GSM>GSM8801825</GSM><GSM>GSM8801803</GSM><GSM>GSM8801826</GSM><GSM>GSM8801804</GSM><GSM>GSM8801805</GSM><GSM>GSM8801827</GSM><GSM>GSM8801828</GSM><GSM>GSM8801806</GSM><GSM>GSM8801807</GSM><GSM>GSM8801829</GSM><GSM>GSM8801808</GSM><GSM>GSM8801809</GSM><GPL>24676</GPL><GSE>289932</GSE><taxon>Homo sapiens</taxon><PMID>[42707060]</PMID></cross_references></HashMap>