ArticlePathobiology of aging & age related diseases2012
Growth hormone, inflammation and aging.
Article in Pathobiology of aging & age related diseases, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 91 citations in OpenAlex.
- Epigenetic Clocks Can Predict Age in the Largemouth Bass-Complex Despite Spatial and Sexual Variation.Evolutionary applications · 2026Article
- Age-related transcriptional drift and physiological adaptation in long-living Ames dwarf skeletal muscle.NAR molecular medicine · 2026Article
- Growing Pains: GH-induced Fibrosis Across Multiple Organs in bGH Mice.Endocrinology · 2025Article
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- MicrobiomeKG: bridging microbiome research and host health through knowledge graphs.Frontiers in systems biology · 2025Article
- The lifespan-extending MEK1 inhibitor trametinib promotes regulation of de novo lipogenesis enzymes by chaperone-mediated autophagy.Frontiers in aging · 2025Article
- Non-pituitary growth hormone enables colon cell senescence evasion.Aging cell · 2024Article
- A Review of the Effects of Some Extrinsic Factors on Mice Used in Research.Comparative medicine · 2023Review
- Identification and validation of aging-related gene signatures and their immune landscape in diabetic nephropathy.Frontiers in medicine · 2023Article
- Article
- Growth hormone increases DNA damage in ovarian follicles and macrophage infiltration in the ovaries.GeroScience · 2022Article
- Rapamycin, Acarbose and 17α-estradiol share common mechanisms regulating the MAPK pathways involved in intracellular signaling and inflammation.Immunity & ageing : I & A · 2022Article
- Article
- Recombinant Human Growth Hormone Inhibits Lipotoxicity, Oxidative Stress, and Apoptosis in a Mouse Model of Diabetic Cardiomyopathy.Oxidative medicine and cellular longevity · 2021Article
- Integrated metabolomics reveals altered lipid metabolism in adipose tissue in a model of extreme longevity.GeroScience · 2020Article
- Effects of GH/IGF on the Aging Mitochondria.Cells · 2020Review
- Lifespan of long-lived growth hormone receptor knockout mice was not normalized by housing at 30°C since weaning.Aging cell · 2020Article
- Challenging a "Cushy" Life: Potential Roles of Thermogenesis and Adipose Tissue Adaptations in Delayed Aging of Ames and Snell Dwarf Mice.Metabolites · 2020Review
- Primordial follicle reserve, DNA damage and macrophage infiltration in the ovaries of the long-living Ames dwarf mice.Experimental gerontology · 2020Article
- Review
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 2 institutions in 2 countries.
Funding
Abstract
Mutant animals characterized by extended longevity provide valuable tools to study the mechanisms of aging. Growth hormone and insulin-like growth factor-1 (IGF-1) constitute one of the well-established pathways involved in the regulation of aging and lifespan. Ames and Snell dwarf mice characterized by GH deficiency as well as growth hormone receptor/growth hormone binding protein knockout (GHRKO) mice characterized by GH resistance live significantly longer than genetically normal animals. During normal aging of rodents and humans there is increased insulin resistance, disruption of metabolic activities and decline of the function of the immune system. All of these age related processes promote inflammatory activity, causing long term tissue damage and systemic chronic inflammation. However, studies of long living mutants and calorie restricted animals show decreased pro-inflammatory activity with increased levels of anti-inflammatory adipokines such as adiponectin. At the same time, these animals have improved insulin signaling and carbohydrate homeostasis that relate to alterations in the secretory profile of adipose tissue including increased production and release of anti-inflammatory adipokines. This suggests that reduced inflammation promoting healthy metabolism may represent one of the major mechanisms of extended longevity in long-lived mutant mice and likely also in the human.
Indexed as
Identifiers
What 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.