ReviewBMB reports2019
Growth signaling and longevity in mouse models.
Review in BMB reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Mitochondrial dynamics in depression: friend or foe?Metabolic brain disease · 2026Review
- Small-molecule IGF1R inhibitors extend healthspan in a mouse model.bioRxiv : the preprint server for biology · 2026Article
- The role of fermented foods in healthy longevity: A review of potential anti-aging mechanisms.Current research in food science · 2026Review
- T-CLASS: An Online Tool for the Identification and Classification of Aging and Senescence Using Transcriptome Data.Aging cell · 2025Article
- Maternal α-casein deficiency extends the lifespan of offspring and programmes their body composition.GeroScience · 2025Article
- Oxidative stress impairs the Nur77-Sirt1 axis resulting in a decline in organism homeostasis during aging.Aging cell · 2023Article
- Molecular inhibition of RAS signalling to target ageing and age-related health.Disease models & mechanisms · 2022Review
- Article
- Role of FoxO transcription factors in aging and age-related metabolic and neurodegenerative diseases.Cell & bioscience · 2021Review
- Neofunctionalization of a second insulin receptor gene in the wing-dimorphic planthopper, Nilaparvata lugens.PLoS genetics · 2021Article
- Insulin: too much of a good thing is bad.BMC medicine · 2020Review
- The World Goes Bats: Living Longer and Tolerating Viruses.Cell metabolism · 2020Review
- Hormesis in Health and Chronic Diseases.Trends in endocrinology and metabolism: TEM · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reduction of insulin/insulin-like growth factor 1 (IGF1) signaling (IIS) extends the lifespan of various species. So far, several longevity mouse models have been developed containing mutations related to growth signaling deficiency by targeting growth hormone (GH), IGF1, IGF1 receptor, insulin receptor, and insulin receptor substrate. In addition, p70 ribosomal protein S6 kinase 1 (S6K1) knockout leads to lifespan extension. S6K1 encodes an important kinase in the regulation of cell growth. S6K1 is regulated by mechanistic target of rapamycin (mTOR) complex 1. The v-myc myelocytomatosis viral oncogene homolog (MYC)-deficient mice also exhibits a longevity phenotype. The gene expression profiles of these mice models have been measured to identify their longevity mechanisms. Here, we summarize our knowledge of long-lived mouse models related to growth and discuss phenotypic characteristics, including organ-specific gene expression patterns. [BMB Reports 2019; 52(1): 70-85].
Indexed as
Identifiers
30545442PMC6386229What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.