Progeroid syndromes: models for stem cell aging?

被引:1
作者
Bellantuono, I. [1 ]
Sanguinetti, G. [2 ]
Keith, W. N. [3 ]
机构
[1] Univ Sheffield, Dept Human Metab, Mellanby Ctr Bone Res, Sheffield, S Yorkshire, England
[2] Univ Edinburgh, Inst Adapt & Neural Computat, Edinburgh, Midlothian, Scotland
[3] Univ Glasgow, Inst Canc Sci, CRUK Beatson Labs, Glasgow, Lanark, Scotland
关键词
Down syndrome; Notch; Wnt; Hematopoietic; Mesenchymal; System biology; RHEUMATOID-ARTHRITIS; DOWNS-SYNDROME; BONE-MARROW; OSTEOBLAST DIFFERENTIATION; TELOMERE DYSFUNCTION; SELF-RENEWAL; MOUSE MODEL; MYELODYSPLASTIC SYNDROMES; MESENCHYMAL PROGENITORS; CHROMOSOMAL INSTABILITY;
D O I
10.1007/s10522-011-9347-2
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
030301 [社会学]; 100201 [内科学];
摘要
Stem cells are responsible for tissue repair and maintenance and it is assumed that changes observed in the stem cell compartment with age underlie the concomitant decline in tissue function. Studies in murine models have highlighted the importance of intrinsic changes occurring in stem cells with age. They have also drawn the attention to other factors, such as changes in the local or systemic environment as the primary cause of stem cell dysfunction. Whilst knowledge in murine models has been advancing rapidly there has been little translation of these data to human aging. This is most likely due to the difficulties of testing the regenerative capacity of human stem cells in vivo and to substantial differences in the aging phenotype within humans. Here we summarize evidence to show how progeroid syndromes, integrated with other models, can be valuable tools in addressing questions about the role of stem cell aging in human degenerative diseases of older age and the molecular pathways involved.
引用
收藏
页码:63 / 75
页数:13
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