NYMC Faculty Publications
DOI
10.1007/s12015-017-9728-2
Journal Title
Stem Cell Reviews and Reports
First Page
443
Last Page
453
Document Type
Article
Publication Date
8-1-2017
Department
Pathology, Microbiology and Immunology
Abstract
The dream of slowing down the aging process has always inspired mankind. Since stem cells are responsible for tissue and organ rejuvenation, it is logical that we should search for encoded mechanisms affecting life span in these cells. However, in adult life the hierarchy within the stem cell compartment is still not very well defined, and evidence has accumulated that adult tissues contain rare stem cells that possess a broad trans-germ layer differentiation potential. These most-primitive stem cells-those endowed with pluripotent or multipotent differentiation ability and that give rise to other cells more restricted in differentiation, known as tissue-committed stem cells (TCSCs) - are of particular interest. In this review we present the concept supported by accumulating evidence that a population of so-called very small embryonic-like stem cells (VSELs) residing in adult tissues positively impacts the overall survival of mammals, including humans. These unique cells are prevented in vertebrates from premature depletion by decreased sensitivity to growth hormone (GH), insulin (INS), and insulin-like growth factor (IGF) signaling, due to epigenetic changes in paternally imprinted genes that regulate their resistance to these factors. In this context, we can envision nutrient response GH/INS/IGF signaling pathway as a lethal factor for these most primitive stem cells and an important culprit in aging.
Recommended Citation
Ratajczak, M., Bartke, A., & Darzynkiewicz, Z. (2017). Prolonged Growth Hormone/Insulin/Insulin-like Growth Factor Nutrient Response Signaling Pathway as a Silent Killer of Stem Cells and a Culprit in Aging. Stem Cell Reviews and Reports, 13 (4), 443-453. https://doi.org/10.1007/s12015-017-9728-2
Publisher's Statement
Originally published in Stem Cell Reviews and Reports, 13 (4), 443-453. The original material can be found here.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.