ReviewMechanisms of ageing and development2008
How does suppression of IGF-1 signaling by DNA damage affect aging and longevity?
Review in Mechanisms of ageing and development, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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
12 citing papers in PubMed, 33 citations in OpenAlex.
- The longevity effects of reduced IGF-1 signaling depend on the stability of the mitochondrial genome.Science advances · 2026Article
- Article
- Compression of morbidity in a progeroid mouse model through the attenuation of myostatin/activin signalling.Journal of cachexia, sarcopenia and muscle · 2019Article
- Chemically induced carcinogenesis in rodent models of aging: assessing organismal resilience to genotoxic stressors in geroscience research.GeroScience · 2019Review
- Excess growth hormone suppresses DNA damage repair in epithelial cells.JCI insight · 2019Article
- Insulin-like growth factor-1 receptor regulates repair of ultraviolet B-induced DNA damage in human keratinocytes in vivo.Molecular oncology · 2016Article
- Astrocyte Resilience to Oxidative Stress Induced by Insulin-like Growth Factor I (IGF-I) Involves Preserved AKT (Protein Kinase B) Activity.The Journal of biological chemistry · 2016Article
- Lifespan and Stress Resistance in Drosophila with Overexpressed DNA Repair Genes.Scientific reports · 2015Article
- Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury.F1000Research · 2014Article
- Axis of ageing: telomeres, p53 and mitochondria.Nature reviews. Molecular cell biology · 2012Review
- Recent insights into the molecular mechanisms involved in aging and the malignant transformation of adult stem/progenitor cells and their therapeutic implications.Ageing research reviews · 2009Review
- Insulin and JNK: optimizing metabolic homeostasis and lifespan.Trends in endocrinology and metabolism: TEM · 2009Review
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 at 1 institution in 1 country.
Funding
Abstract
Long-lived animals have evolved a robust set of defenses to maintain genomic integrity over their entire lifespan. The DNA damage response and DNA repair pathways are critical pillars of organismal defenses, minimizing somatic mutations in both post-mitotic and mitotic cells. These genomic maintenance systems not only prevent the premature emergence of cancers but may also maintain normal tissue function and organismal longevity. Genetic defects in a number of DNA repair and DNA damage response genes often leads to a dramatic increase in cancer incidence; in other cases, premature aging or progeroid syndromes may be induced. In this review, we discuss two recent reports of two nucleotide excision repair-deficient models that exhibit dramatic premature aging and shortened longevity. The DNA repair defects were also associated with a significant inhibition of the growth hormone/insulin-like growth factor 1 (GH/IGF-1) axis, an endocrine signaling pathway shown to influence aging and longevity in both vertebrates and invertebrates. Potential mechanisms of how DNA damage might affect IGF-1 signaling and aging are discussed, with a particular emphasis on the role of such signaling alterations in the adult tissue stem cell compartments.
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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.