Deficiencies in DNA damage repair limit the function of haematopoietic stem cells with age

By Derrick J. Rossi, David Bryder, J. Seita, A. Nussenzweig, Jan H. J. Hoeijmakers, Irving L. Weissman. Nature, 2007

1,124 citations recorded by the source corpus.

Subfields: Hematology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/2e75cdbc469053668810df7f2d34500ea1da3c13

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Hematology

1. S. Morrison
2. Derrick J. Rossi
3. G. Semenza
4. Irving L. Weissman
5. T. Suda
6. Catriona H. M. Jamieson
7. David Bryder
8. E. Passegué

In Molecular Biology

1. Irving L. Weissman
2. Stephen P. Jackson
3. S. Morrison
4. Derrick J. Rossi
5. J. Bartek
6. Guido Kroemer
7. Linda Partridge
8. Shenghui He

In Physiology

1. Manuel Serrano
2. Guido Kroemer
3. Linda Partridge
4. S. Morrison
5. M. Blasco
6. C. López‐Otín
7. Derrick J. Rossi
8. T. Suda

Citations in the corpus

• The DNA-damage response in human biology and disease (2009, background): “Indeed, defects in base-excision repair, NER, mismatch repair, HR or the Fanconi anaemia complex impair stem-cell function 47 , and NER or NHEJ defects trigger age-related haematopoietic stem-cell failure in mice 48,49 .”
• Functionally distinct hematopoietic stem cells modulate hematopoietic lineage potential during aging by a mechanism of clonal expansion (2010, methodology): “HSCs were isolated, and competitive transplants were performed as previously described (33).”
• The hallmarks of aging. (2013, background): “Consequences of the exhaustion of hematopoietic stem cells (HSCs), mesenchymal stem cells (MSCs), satellite cells, and intestinal epithelial stem cells (IESCs) are exemplified.”
• Oxidative Stress, Mitochondrial Dysfunction, and Aging (2011, background): “HSCs in mice deficient in DNA repair pathways, including nucleotide excision repair, telomere maintenance, and nonhomologous end-joining, exhibit increased sensitivity to the detrimental effect of ROS, diminished self-renewal and functional exhaustion with age [103].”
• Mechanisms of stem cell self-renewal. (2009, background): “The loss of telomerase activity reduces the self-renewal potential of HSCs upon serial transplantation (Allsopp et al. 2003), their functional capacity during aging (Rossi et al. 2007), and the regenerative capacity of other tissues (Herrera et al. 1999, Lee et al. 1998).”
• Stems cells and the pathways to aging and cancer. (2008, background): “These results suggest that quiescence itself might be a critical factor involved in facilitating the accrual of DNA damage in stem cells (Rossi et al., 2007c).”
• Metabolic regulation of hematopoietic stem cells in the hypoxic niche. (2011, background): “Such error-prone repair may contribute to stem cell senescence, apoptosis, and leukemic transformation (Rossi et al., 2007, 2008).”
• Hematopoietic stem cell quiescence promotes error prone DNA repair and mutagenesis (2010, background): “In terms of organ maintenance, it is logical to keep long-lived HSCs quiescent in vivo to guard them against DNA replication errors and damage associated with oxidative stress (Rossi et al., 2007; Orford and Scadden, 2008).”