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The Role of the IGF Axis in Disease, 4th Edition
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The Role of the IGF Axis in Disease, 4th Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 20 August 2025 | Viewed by 3006

Special Issue Editor

Dr. Claire M. Perks

E-Mail Website
Guest Editor
Cancer Endocrinology Group, Bristol Medical School, Southmead Hospital, Bristol BS10 5NB, UK
Interests: metabolic disturbances; IGFs and epithelial cancers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue continues on from our previous Special Issues, "The Role of the IGF Axis in Disease", “The Role of the IGF Axis in Disease 2.0”, and “The Role of the IGF Axis in Disease, 3nd Edition”.

This research topic aims to highlight the key roles that members of the insulin-like growth factor (IGF) axis (including ligands, IGF-I and -II, IGF binding proteins (IGFBPs1-6) and IGF receptors) play in the risk and development of diseases. The IGF family can affect many physiological systems in the body by modulating cell processes, including proliferation, differentiation, survival, and metabolism. Consequently, they are often dysregulated in many pathological conditions, leading to the development of different strategies to target them.

Dr. Claire M. Perks
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • IGF axis
  • cancer
  • obesity
  • hallmarks of cancer

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Published Papers (3 papers)

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Research

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14 pages, 729 KiB  
Article
Serum Insulin-like Growth Factor-II Is Associated with Poor Poststroke Outcomes in Males: A Secondary Analysis
by Christian Glamheden, N. David Åberg, Gustaf Gadd and Daniel Åberg
Int. J. Mol. Sci. 2025, 26(12), 5525; https://doi.org/10.3390/ijms26125525 - 9 Jun 2025
Viewed by 75
Abstract
The insulin-like growth factor (IGF) system has significance for poststroke outcomes. Previously, we reported that low serum IGF-II (s-IGF-II) in the acute phase is associated with poststroke mortality, and that IGF-II is lower among males. Given the known interactions of the IGF system [...] Read more.
The insulin-like growth factor (IGF) system has significance for poststroke outcomes. Previously, we reported that low serum IGF-II (s-IGF-II) in the acute phase is associated with poststroke mortality, and that IGF-II is lower among males. Given the known interactions of the IGF system and estrogen receptor signaling, s-IGF-II may have sex-specific effects. In this study, we conducted a secondary analysis of sex differences in s-IGF-II and poststroke functional outcomes and mortality after ischemic stroke (IS) in the Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS, males; n = 315, females; n = 177). Functional outcomes were assessed using the modified Rankin scale (mRS) at 3 months and 2 years poststroke. Survival was recorded for 7 years or until death. Males in the lowest quintile of acute s-IGF-II had a higher poststroke mortality, with a crude hazard ratio [HR] of 2.52 (95% confidence interval [CI]) 1.59–3.99) and an adjusted HR of 1.83 (95% CI 1.09–3.06). No corresponding significant association was observed in females. Although acute s-IGF-II was crudely associated with poor functional outcomes among males after 3 months and 2 years, these associations were not independent of initial stroke severity in adjusted models. In conclusion, low levels of acute s-IGF-II are linked with poststroke mortality among males, but not significantly in females. Further studies are, however, warranted with sex hormone analysis, consideration of specific cause of death, and more females. Full article
(This article belongs to the Special Issue The Role of the IGF Axis in Disease, 4th Edition)
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15 pages, 1708 KiB  
Article
Insulin Receptor Substrate-2 Regulates the Secretion of Growth Factors in Response to Amino Acid Deprivation
by Ayaka Takahashi, Haruka Furuta, Hiroki Nishi, Hiroyasu Kamei, Shin-Ichiro Takahashi and Fumihiko Hakuno
Int. J. Mol. Sci. 2025, 26(2), 841; https://doi.org/10.3390/ijms26020841 - 20 Jan 2025
Viewed by 992
Abstract
Insulin receptor substrates (IRSs) are well-known mediators of the insulin and insulin-like growth factor (IGF)-I signaling pathways. We previously reported that the protein levels of IRS-2, a molecular species of IRS, were upregulated in the livers of rats fed a protein-restricted diet. This [...] Read more.
Insulin receptor substrates (IRSs) are well-known mediators of the insulin and insulin-like growth factor (IGF)-I signaling pathways. We previously reported that the protein levels of IRS-2, a molecular species of IRS, were upregulated in the livers of rats fed a protein-restricted diet. This study aimed to elucidate the physiological role of IRS-2, whose level increases in response to protein restriction in cultured hepatocyte models. Hepatocyte-derived cell lines subjected to amino acid deprivation showed increased IRS2 mRNA and IRS-2 protein levels due to increased IRS2 transcription and translation, respectively. Amino acid deprivation markedly increased vascular endothelial growth factor-D (VEGF-D) secretion. Remarkably, the amino acid deprivation-induced VEGF-D secretion was suppressed by IRS-2 knockdown and enhanced by IRS-2 overexpression. These results suggest that IRS-2 is an intercellular signaling molecule that extracellularly transmits information on amino acid deprivation stress by regulating the secretion of growth factors such as VEGF-D. Moreover, this function of IRS-2 is distinct from its currently accepted function as a mediator of the insulin/IGF-I signaling pathways. This study demonstrates that IRS-2 can modulate protein secretion in an insulin-independent manner and greatly expands our understanding of the role of IRS-2, which is upregulated in response to amino acid deprivation. Full article
(This article belongs to the Special Issue The Role of the IGF Axis in Disease, 4th Edition)
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Review

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30 pages, 2663 KiB  
Review
IGFBP-2 and IGF-II: Key Components of the Neural Stem Cell Niche? Implications for Glioblastoma Pathogenesis
by Abigail J. Harland and Claire M. Perks
Int. J. Mol. Sci. 2025, 26(10), 4749; https://doi.org/10.3390/ijms26104749 - 15 May 2025
Viewed by 531
Abstract
Glioblastoma is a fatal and aggressive cancer with no cure. It is becoming increasingly clear that glioblastoma initiation is a result of adult neural stem cell (NSC) transformation—most likely those within the subventricular zone (SVZ). Indeed, transcriptomic analysis indicates that glioblastomas are reminiscent [...] Read more.
Glioblastoma is a fatal and aggressive cancer with no cure. It is becoming increasingly clear that glioblastoma initiation is a result of adult neural stem cell (NSC) transformation—most likely those within the subventricular zone (SVZ). Indeed, transcriptomic analysis indicates that glioblastomas are reminiscent of a neurodevelopmental hierarchy, in which neural stem and progenitor markers are widely expressed by tumour stem-like cells. However, NSC fates and the cues that drive them are poorly understood. Studying the crosstalk within NSC niches may better inform our understanding of glioblastoma initiation and development. Insulin-like growth factor binding protein 2 (IGFBP-2) has a well-established prognostic role in glioblastoma, and cell-based mechanistic studies show the independent activation of downstream oncogenic pathways. However, IGFBP-2 is more commonly recognised as a modulator of insulin-like growth factors (IGFs) for receptor tyrosine kinase signal propagation or attenuation. In the adult human brain, both IGFBP-2 and IGF-II expression are retained in the choroid plexus (ChP) and secreted into the cerebral spinal fluid (CSF). Moreover, secretion by closely associated cells and NSCs themselves position IGFBP-2 and IGF-II as interesting factors within the NSC niche. In this review, we will highlight the experimental findings that show IGFBP-2 and IGF-II influence NSC behaviour. Moreover, we will link this to glioblastoma biology and demonstrate the requirement for further analysis of these factors in glioma stem cells (GSCs). Full article
(This article belongs to the Special Issue The Role of the IGF Axis in Disease, 4th Edition)
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