The DOI matches its Crossref record; 111 of the 112 references it cites were found in a registry or an index.
The GH/IGF1 axis and signaling pathways in the muscle and bone: mechanisms underlying age-related skeletal muscle wasting and osteoporosis
Open accessAbstract
The widespread increase in life expectancy is accompanied by an increased prevalence of features of physical frailty. Signs and symptoms may include sarcopenia and osteopenia, reduced exercise capacity, and diminished sense of well-being. The pathogenesis of age-associated sarcopenia and osteopenia is multifactorial, and hormonal decline may be a contributing factor. Aging is associated with a progressive decrease in GH secretion, and more than 30% of elderly people have circulating IGF1 levels below the normal range found in the young. GH acts directly on target tissues, including skeletal muscle and bone among many others, but many effects are mediated indirectly by circulating (liver-derived) or locally produced IGF1. Aging is also associated with reduced insulin sensitivity which, in turn, may contribute to the impairment of IGF1 action. Recent experimental evidence suggests that besides the age-dependent decline in GH and IGF1 serum levels, the dysregulation of GH and IGF1 actions due to impairment of the post-receptor signaling machinery may contribute to the loss of muscle mass and osteopenia. This article will focus on the molecular mechanisms of impaired GH and IGF1 signaling and action in aging, and their role in the pathogenesis of sarcopenia and osteoporosis.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Increased adiposity and circulating concentrations of free fatty acids inhibit GH production and decrease plasma concentrations of IGF-1.”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [93]
In the citing paper
“This decrease in IGF-1 is associated with decreased muscle size and strength, decreased protein synthesis, and increased cell death,93 which in turn leads to increased visceral fat and decreased lean body mass.94”
From Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases (2014) · cites this paper as [93]
In the citing paper
“GH acts both directly on bones and indirectly through liver-derived IGF-1 or locally produced IGF-1 [47].”
From Emerging role of liver-bone axis in osteoporosis (2024) · cites this paper as [47]
In the citing paper
“The growth hormone (GH)-IGF-1 axis is also involved in bone remodeling and metabolism and has an essential role in the achievement and maintenance of bone mass throughout life.”
From Emerging role of liver-bone axis in osteoporosis (2024) · cites this paper as [47]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Biochemical and Biophysical Research Communications
Rc, A. N., On Filamentous Bacteriophage, M., Hoffmann, S., & Willbold, D. (1960) · Nature · doi:10.1038/186124d0 · Cited by 6,690
Regulation of skeletal muscle mass in mice by a new TGF-p superfamily member
McPherron, A. C., Lawler, A. M., & Lee, S.-J. (1997) · Nature · doi:10.1038/387083a0 · Cited by 4,013
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
Hoskins, R. G. (1953) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jcem-13-4-473 · Cited by 3,780
The American journal of clinical nutrition
(1993) · Journal of the American Dietetic Association · doi:10.1016/0002-8223(93)92305-h · Cited by 3,316
Sandri, M., Sandri, C., Gilbert, A., Skurk, C., Calabria, E., Picard, A., Walsh, K., Schiaffino, S., Lecker, S. H., & Goldberg, A. L. (2004) · Cell · doi:10.1016/s0092-8674(04)00400-3 · Cited by 3,012
Bodine, S. C., Stitt, T. N., Gonzalez, M., Kline, W. O., Stover, G. L., Bauerlein, R., Zlotchenko, E., Scrimgeour, A., Lawrence, J. C., Glass, D. J., et al. (2001) · Nature Cell Biology · doi:10.1038/ncb1101-1014 · Cited by 2,752
Role of insulin-like growth factors in embryonic and postnatal growth
Baker, J., Liu, J.-P., Robertson, E. J., & Efstratiadis, A. (1993) · Cell · doi:10.1016/s0092-8674(05)80085-6 · Cited by 2,463
Comfortable and maximum walking speed of adults aged 20—79 years: reference values and determinants
Bohannon, R. W. (1997) · Age and Ageing · doi:10.1093/ageing/26.1.15 · Cited by 2,346
Cellular and Molecular Life Sciences
(2013) · Cellular and Molecular Life Sciences · doi:10.1007/18.1420-9071 · Cited by 1,804
The p66shc adaptor protein controls oxidative stress response and life span in mammals
Migliaccio, E., Giorgio, M., Mele, S., Pelicci, G., Reboldi, P., Pandolfi, P. P., Lanfrancone, L., & Pelicci, P. G. (1999) · Nature · doi:10.1038/46311 · Cited by 1,712
Cited by
Sorted by citations
Muscle–Organ Crosstalk: The Emerging Roles of Myokines
Severinsen, M. C. K., & Pedersen, B. K. (2020) · Endocrine Reviews · doi:10.1210/endrev/bnaa016 · Cited by 1,226
“Muscle-derived IGF-1 can act on local osteoblasts that express the IGF-1 receptor and thereby promote bone formation (171).”
BackgroundSkeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1
Bodine, S. C., & Baehr, L. M. (2014) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00204.2014 · Cited by 1,159
Age-related and disease-related muscle loss: The effect of diabetes, obesity, and other diseases
Kalyani, R. R., Corriere, M., & Ferrucci, L. (2014) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(14)70034-8 · Cited by 1,102
The p53 network: cellular and systemic DNA damage responses in aging and Cancer
Reinhardt, H. C., & Schumacher, B. (2012) · Trends in Genetics · doi:10.1016/j.tig.2011.12.002 · Cited by 458
Dietary Advanced Glycation End Products and Aging
Luevano-Contreras, C., & Chapman-Novakofski, K. (2010) · Nutrients · doi:10.3390/nu2121247 · Cited by 396
Metadata
- Authors
- Perrini, S., Laviola, L., Carreira, M. C., Cignarelli, A., Natalicchio, A., & Giorgino, F.
- Affiliations
- University of Bari Aldo Moro (IT)
- ORCID
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2010-03-02
- Volume
- 205
- Issue
- 3
- Pages
- 201-210
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W2132915404
- Cited by
- 317
- References
- 112
- Citations by year
- 2026: 8 · 2025: 11 · 2024: 13 · 2023: 12 · 2022: 17 · 2021: 18 · 2020: 14 · 2019: 15 · 2018: 23 · 2017: 17 · 2016: 25 · 2015: 23 · 2014: 29 · 2013: 27 · 2012: 36
- FWCI
- 4.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- INFM-OAR (INFN Catania) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Growth Hormone and Insulin-like Growth Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology (medical) › Nutrition and Health in Aging
- Keywords
- growth hormone, insulin-like growth factor I, somatotropic axis, sarcopenia, osteoporosis, osteopenia, aging, muscle atrophy, bone loss, insulin resistance, post-receptor signaling, frailty, skeletal muscle, bone
- MeSH terms
- Animals, Bone and Bones, Disease Models, Animal, Humans, Insulin-Like Growth Factor I, Osteoporosis, Growth Hormone, Signal Transduction, Muscle, Skeletal, Sarcopenia
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
