Matches in SemOpenAlex for { <https://semopenalex.org/work/W4306651808> ?p ?o ?g. }
- W4306651808 endingPage "3260" @default.
- W4306651808 startingPage "3260" @default.
- W4306651808 abstract "The growth hormone (GH)-insulin-like growth factor-1 (IGF1) signaling pathway plays a major role in orchestrating cellular interactions, metabolism, growth and aging. Studies from worms to mice showed that downregulated activity of the GH/IGF1 pathway could be beneficial for the extension of lifespan. Laron syndrome (LS) is an inherited autosomal recessive disorder caused by molecular defects of the GH receptor (GHR) gene, leading to congenital IGF1 deficiency. Life-long exposure to minute endogenous IGF1 levels in LS is associated with low stature as well as other endocrine and metabolic deficits. Epidemiological surveys reported that patients with LS have a reduced risk of developing cancer. Studies conducted on LS-derived lymphoblastoid cells led to the identification of a novel link between IGF1 and thioredoxin-interacting protein (TXNIP), a multifunctional mitochondrial protein. TXNIP is highly expressed in LS patients and plays a critical role in cellular redox regulation by thioredoxin. Given that IGF1 affects the levels of TXNIP under various stress conditions, including high glucose and oxidative stress, we hypothesized that the IGF1-TXNIP axis plays an essential role in helping maintain a physiological balance in cellular homeostasis. In this study, we show that TXNIP is vital for the cell fate choice when cells are challenged by various stress signals. Furthermore, prolonged IGF1 treatment leads to the establishment of a premature senescence phenotype characterized by a unique senescence network signature. Combined IGF1/TXNIP-induced premature senescence can be associated with a typical secretory inflammatory phenotype that is mediated by STAT3/IL-1A signaling. Finally, these mechanistic insights might help with the understanding of basic aspects of IGF1-related pathologies in the clinical setting." @default.
- W4306651808 created "2022-10-18" @default.
- W4306651808 creator A5003904670 @default.
- W4306651808 creator A5024749019 @default.
- W4306651808 creator A5033881645 @default.
- W4306651808 creator A5090768607 @default.
- W4306651808 date "2022-10-17" @default.
- W4306651808 modified "2023-10-14" @default.
- W4306651808 title "Long-Term IGF1 Stimulation Leads to Cellular Senescence via Functional Interaction with the Thioredoxin-Interacting Protein, TXNIP" @default.
- W4306651808 cites W102166461 @default.
- W4306651808 cites W1518494023 @default.
- W4306651808 cites W1820314031 @default.
- W4306651808 cites W1931961097 @default.
- W4306651808 cites W1965883826 @default.
- W4306651808 cites W1966164727 @default.
- W4306651808 cites W1966453709 @default.
- W4306651808 cites W1968994105 @default.
- W4306651808 cites W1969760191 @default.
- W4306651808 cites W1970563875 @default.
- W4306651808 cites W1977709885 @default.
- W4306651808 cites W1983323920 @default.
- W4306651808 cites W1984533078 @default.
- W4306651808 cites W1985594739 @default.
- W4306651808 cites W1990815825 @default.
- W4306651808 cites W1993524465 @default.
- W4306651808 cites W1993541144 @default.
- W4306651808 cites W1997184178 @default.
- W4306651808 cites W2002239849 @default.
- W4306651808 cites W2007244362 @default.
- W4306651808 cites W2020636054 @default.
- W4306651808 cites W2023460369 @default.
- W4306651808 cites W2024837178 @default.
- W4306651808 cites W2025651276 @default.
- W4306651808 cites W2028490033 @default.
- W4306651808 cites W2038652783 @default.
- W4306651808 cites W2042281196 @default.
- W4306651808 cites W2043998802 @default.
- W4306651808 cites W2044909936 @default.
- W4306651808 cites W2053736563 @default.
- W4306651808 cites W2054016503 @default.
- W4306651808 cites W2057497222 @default.
- W4306651808 cites W2065351002 @default.
- W4306651808 cites W2071910975 @default.
- W4306651808 cites W2077180087 @default.
- W4306651808 cites W2084967524 @default.
- W4306651808 cites W2087404852 @default.
- W4306651808 cites W2089527908 @default.
- W4306651808 cites W2093055261 @default.
- W4306651808 cites W2097502952 @default.
- W4306651808 cites W2107277218 @default.
- W4306651808 cites W2111843196 @default.
- W4306651808 cites W2114867673 @default.
- W4306651808 cites W2117350664 @default.
- W4306651808 cites W2122379933 @default.
- W4306651808 cites W2132403739 @default.
- W4306651808 cites W2135873477 @default.
- W4306651808 cites W2139847445 @default.
- W4306651808 cites W2140513457 @default.
- W4306651808 cites W2140930678 @default.
- W4306651808 cites W2150932906 @default.
- W4306651808 cites W2156136676 @default.
- W4306651808 cites W2167660024 @default.
- W4306651808 cites W2169840370 @default.
- W4306651808 cites W2174361280 @default.
- W4306651808 cites W2191745121 @default.
- W4306651808 cites W2192080449 @default.
- W4306651808 cites W2336229842 @default.
- W4306651808 cites W2336451601 @default.
- W4306651808 cites W2347124184 @default.
- W4306651808 cites W2424236546 @default.
- W4306651808 cites W2559958687 @default.
- W4306651808 cites W2567472367 @default.
- W4306651808 cites W2584289628 @default.
- W4306651808 cites W2587039580 @default.
- W4306651808 cites W2613674801 @default.
- W4306651808 cites W2614085889 @default.
- W4306651808 cites W2659277361 @default.
- W4306651808 cites W2749511637 @default.
- W4306651808 cites W2752668646 @default.
- W4306651808 cites W2761287732 @default.
- W4306651808 cites W2783939587 @default.
- W4306651808 cites W2789542398 @default.
- W4306651808 cites W2791758888 @default.
- W4306651808 cites W2791866166 @default.
- W4306651808 cites W2797389850 @default.
- W4306651808 cites W2800736744 @default.
- W4306651808 cites W2801193436 @default.
- W4306651808 cites W2801198233 @default.
- W4306651808 cites W2804802143 @default.
- W4306651808 cites W2807914406 @default.
- W4306651808 cites W2891688761 @default.
- W4306651808 cites W2900136751 @default.
- W4306651808 cites W2903003302 @default.
- W4306651808 cites W2911410551 @default.
- W4306651808 cites W2911642321 @default.
- W4306651808 cites W2912063221 @default.
- W4306651808 cites W2918171088 @default.
- W4306651808 cites W2924622926 @default.