ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2011
Single-gene mutations and healthy ageing in mammals.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 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.
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Who cites it
62 citing papers in PubMed, 110 citations in OpenAlex.
- Discovery of novel non-synonymous SNP variants in 988 candidate genes from 6 centenarians by target capture and next-generation sequencing.Mechanisms of ageing and development · 2013Trial
- Discrimination of normal from slow-aging mice by plasma metabolomic and proteomic features.GeroScience · 2026Article
- Harnessing gut microbiota for longevity: Insights into mechanisms and genetic manipulation.iMetaOmics · 2024Article
- Integrated in silico analysis of LRP2 mutations to immunotherapy efficacy in pan-cancer cohort.Discover oncology · 2022Article
- New Directions in Research on Aging.Stem cell reviews and reports · 2022Article
- Somatotropic Axis, Pace of Life and Aging.Frontiers in endocrinology · 2022Review
- Early Life Interventions Can Shape Aging.Frontiers in endocrinology · 2022Review
- Benefits of Living Without Growth Hormone.The journals of gerontology. Series A, Biological sciences and medical sciences · 2021Article
- Extending lifespan by modulating the growth hormone/insulin-like growth factor-1 axis: coming of age.Pituitary · 2021Review
- Transcriptomic profiling of long- and short-lived mutant mice implicates mitochondrial metabolism in ageing and shows signatures of normal ageing in progeroid mice.Mechanisms of ageing and development · 2021Article
- Growth hormone and aging.Reviews in endocrine & metabolic disorders · 2021Review
- Effect of growth hormone on insulin signaling.Molecular and cellular endocrinology · 2020Review
- Canagliflozin extends life span in genetically heterogeneous male but not female mice.JCI insight · 2020Article
- Betaine-rich sugar beet molasses protects from homocysteine-induced reduction of survival in Caenorhabditis elegans.European journal of nutrition · 2020Article
- Stress Resistance Screen in a Human Primary Cell Line Identifies Small Molecules That Affect Aging Pathways and ExtendG3 (Bethesda, Md.) · 2020Article
- Mice with hyper-long telomeres show less metabolic aging and longer lifespans.Nature communications · 2019Article
- Growth Hormone Deficiency: Health and Longevity.Endocrine reviews · 2019Review
- Growth Hormone and Aging: Updated Review.The world journal of men's health · 2019Review
- Impact of Growth Hormone-Related Mutations on Mammalian Aging.Frontiers in genetics · 2018Review
- Article
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Studies of the effects of single-gene mutations on longevity in Caenorhabditis elegans, Drosophila melanogaster and Mus musculus identified homologous, highly conserved signalling pathways that influence ageing. In each of these very distantly related species, single mutations which lead-directly or indirectly-to reduced insulin, insulin-like growth factor (IGF) or insulin/IGF-like signalling (IIS) can produce significant increases in both average and maximal lifespan. In mice, most of the life-extending mutations described to date reduce somatotropic (growth hormone (GH) and IGF-1) signalling. The reported extensions of longevity are most robust in GH-deficient and GH-resistant mice, while suppression of somatotropic signalling 'downstream' of the GH receptor produces effects that are generally smaller and often limited to female animals. This could be due to GH influencing ageing by both IGF-1-mediated and IGF-1-independent mechanisms. In mutants that have been examined in some detail, increased longevity is associated with various indices of delayed ageing and extended 'healthspan'. The mechanisms that probably underlie the extension of both lifespan and healthspan of these animals include increased stress resistance, improved antioxidant defences, alterations in insulin signalling (e.g. hypoinsulinaemia combined with improved insulin sensitivity in some mutants and insulin resistance in others), a shift from pro- to anti-inflammatory profile of circulating adipokines, reduced mammalian target of rapamycin-mediated translation and altered mitochondrial function including greater utilization of lipids when compared with carbohydrates.
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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.