GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE346nnn/GSE346052/primaryOK200OtherMus musculusOtherhttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE346052GEOGSEfalseIntegrated long-read transcriptomics of aging mouse pituitary reveals Pou1f1 vulnerability and novel isoform remodelingAging is a multifactorial process accompanied by profound alterations in endocrine function, which plays a central role in maintaining whole-body physiology and metabolism. Although age-related changes in pituitary hormone levels, including growth hormone (GH), have been documented, the molecular mechanisms underlying pituitary aging and its effects on full-length transcript isoforms remain poorly understood. Here, we performed full-length long-read transcriptomic sequencing (Iso-Seq) of anterior pituitary glands from young and old male mice to comprehensively characterize aging-associated changes in gene expression, isoform usage, and alternative splicing. Integration of differential expression, isoform-switch, and novel isoform analyses identified Pou1f1 as the most significantly downregulated gene in aged pituitaries (log₂FC = −2.02, Padj = 1.02 × 10⁻³⁰), accompanied by reduced expression of genes involved in neurosecretory function, including Syn1, Syt7, Dvl3, and Cacna2d2. Notably, aging was associated with a directional accumulation of novel isoforms, with more isoforms enriched in old than young pituitaries (100 vs. 55; binomial P = 0.0004), together with a global shift toward shorter 3′ UTRs (9.6% reduction in length). Together, these findings provide a high-resolution full-length transcriptomic landscape of pituitary aging and reveal previously unrecognized changes in transcript isoform composition and 3′ UTR architecture that may contribute to age-related endocrine dysfunction.2026/09/08GSE346052GSM1002230234585346052Mus musculus