Author
Listed:
- Kai Mao
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Gabriela Farias Quipildor
(Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Tahmineh Tabrizian
(Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Ardijana Novaj
(Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Fangxia Guan
(Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Ryan O. Walters
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Fabien Delahaye
(Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Gene B. Hubbard
(University of Texas Health Science Center at San Antonio)
- Yuji Ikeno
(University of Texas Health Science Center at San Antonio
Audie L. Murphy Memorial VA Hospital)
- Keisuke Ejima
(The University of Alabama at Birmingham
Indiana University)
- Peng Li
(The University of Alabama at Birmingham)
- David B. Allison
(The University of Alabama at Birmingham
Indiana University)
- Hossein Salimi-Moosavi
(Amgen Inc.)
- Pedro J. Beltran
(Oncology Research, Amgen Inc.)
- Pinchas Cohen
(University of Southern California)
- Nir Barzilai
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
- Derek M. Huffman
(Albert Einstein College of Medicine
Albert Einstein College of Medicine
Albert Einstein College of Medicine)
Abstract
Diminished growth factor signaling improves longevity in laboratory models, while a reduction in the somatotropic axis is favorably linked to human aging and longevity. Given the conserved role of this pathway on lifespan, therapeutic strategies, such as insulin-like growth factor-1 receptor (IGF-1R) monoclonal antibodies (mAb), represent a promising translational tool to target human aging. To this end, we performed a preclinical study in 18-mo-old male and female mice treated with vehicle or an IGF-1R mAb (L2-Cmu, Amgen Inc), and determined effects on aging outcomes. Here we show that L2-Cmu preferentially improves female healthspan and increases median lifespan by 9% (P = 0.03) in females, along with a reduction in neoplasms and inflammation (P ≤ 0.05). Thus, consistent with other models, targeting IGF-1R signaling appears to be most beneficial to females. Importantly, these effects could be achieved at advanced ages, suggesting that IGF-1R mAbs could represent a promising therapeutic candidate to delay aging.
Suggested Citation
Kai Mao & Gabriela Farias Quipildor & Tahmineh Tabrizian & Ardijana Novaj & Fangxia Guan & Ryan O. Walters & Fabien Delahaye & Gene B. Hubbard & Yuji Ikeno & Keisuke Ejima & Peng Li & David B. Allison, 2018.
"Late-life targeting of the IGF-1 receptor improves healthspan and lifespan in female mice,"
Nature Communications, Nature, vol. 9(1), pages 1-12, December.
Handle:
RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04805-5
DOI: 10.1038/s41467-018-04805-5
Download full text from publisher
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04805-5. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.