The DOI matches its Crossref record; 128 of the 128 references it cites were found in a registry or an index; none of the 123 sources its claims cite is checked for support yet.
The telomere syndromes
Open accessAbstract
There has been mounting evidence of a causal role for telomere dysfunction in a number of degenerative disorders. Their manifestations encompass common disease states such as idiopathic pulmonary fibrosis and bone marrow failure. Although these disorders seem to be clinically diverse, collectively they comprise a single syndrome spectrum defined by the short telomere defect. Here we review the manifestations and unique genetics of telomere syndromes. We also discuss their underlying molecular mechanisms and significance for understanding common age-related disease processes.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“There has been mounting evidence of a causal role for telomere dysfunction in a number of degenerative disorders.”
- Also stated in: § Abstract · boosted
“This Review highlights how recent discoveries in human genetics have synergized with the field of telomere biology to unequivocally establish a causal role for telomere dysfunction in several specific, common and recognizable disease contexts.”
§ The telomere syndromes > Abstract
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In the paper
“Among these, the lung disease idiopathic pulmonary fibrosis (IPF) — best known until recently by its ‘idiopathic’ adjective — is the most common manifestation of telomere-mediated disease12.”
§ The telomere syndromes > Abstract
What the sources say
- Not checked yetcites [12] Armanios, M. Telomerase and idiopathic pulmonary fibrosis. Mutat. Res. 730, 52–58 (2012). source
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In the paper
“Because, as we discuss, telomere length is heritable, the unique inheritance patterns that distinguish these syndromes from other Mendelian disorders are also discussed.”
- Also stated in: § Heritability of telomere length in humans · plain
“These observations collectively support that telomere length is a genetically determined trait and that short telomeres are probably sufficient to cause disease phenotypes within similar thresholds to those seen in monogenic disorders.”
§ The telomere syndromes > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Heritability of telomere length in humans · plain
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These observations collectively support that telomere length is a genetically determined trait and that short telomeres are probably sufficient to cause disease phenotypes within similar thresholds to those seen in monogenic disorders.”
§ The telomere syndromes > Telomere length is a heritable trait > Heritability of telomere length in humans
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In the paper
“Mutations in TERT and TR are the most commonly identifiable defects in monogenic telomere syndromes.”
§ The telomere syndromes > Genotype–phenotype correlations > Telomere length is a modifier of disease severity
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIn the paper
“Although these disorders seem to be clinically diverse, collectively they comprise a single syndrome spectrum defined by the short telomere defect.”
- Also stated in: § Abstract · hedged
“Because of their overlapping clinical features, it has been proposed to consider them as a single syndrome spectrum13, and here we refer to them as ‘the telomere syndromes.’”
§ The telomere syndromes > Abstract
What the sources say
- Not checked yetcites [13] Armanios, M. Syndromes of telomere shortening. Annu. Rev. Genom. Hum. Genet. 10, 45–61 (2009). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Rests on an assumption: The short telomere defect in affected individuals is present in germ cells and thus simultaneously affects multiple organs even when one disease presentation predominates.
- Also stated in: § Abstract · hedged
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In the paper
“As described below, mutations in the genes that encode the essential telomerase components — namely, TERT, TR and DKC1 — are a common cause of human telomere syndromes.”
§ The telomere syndromes > Telomeres and telomerase > Telomerase structure
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesA conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“We propose that at least three primary mechanisms explain the diverse telomere-mediated disease phenotypes.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease
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In the paper
“Clinically, this is most apparent in the high penetrance of pulmonary disease in telomerase mutation carriers, even though the lung has a slow mitotic rate56,99.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease
What the sources say
- Not checked yetcites [56] Armanios, M. Y. et al. Telomerase mutations in families with idiopathic pulmonary fibrosis. N. Engl. J. Med. 356, 1317–1326 (2007). References 54–56 showed that lymphocyte telomere length using flow cytometry and fluorescence in situ hybridization could be a useful diagnostic marker in identifying individuals with telomere-related disease. source
- Not checked yetcites [99] Alder, J. K. et al. Telomere length is a determinant of emphysema susceptibility. Am. J. Respir. Crit. Care Med. 183, 904–912 (2011). source
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In the paper
“Altogether, mutations in four genes — DKC1, TINF2, TERT and TR — account for most dyskeratosis congenita cases with an identifiable genetic defect.”
§ The telomere syndromes > The monogenic telomere disorders > Childhood-onset telomere disorders
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- It may state two separate claims as one. 23
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In the paper
“They manifest in an autosomal-dominant inheritance pattern because complete or partial loss-of-function of one allele is sufficient to perturb telomere maintenance38,39,41.”
§ The telomere syndromes > Genotype–phenotype correlations > Telomere length is a modifier of disease severity
What the sources say
- Not checked yetcites [38] Vulliamy, T. et al. The RNA component of telomerase is mutated in autosomal dominant dyskeratosis congenita. Nature 413, 432–435 (2001). source
- Not checked yetcites [39] Armanios, M. et al. Haploinsufficiency of telomerase reverse transcriptase leads to anticipation in autosomal dominant dyskeratosis congenita. Proc. Natl Acad. Sci. USA 102, 15960–15964 (2005). References 38 and 39 identified mutations in the essential telomerase genes, TERT and TR , in dyskeratosis congenita. source
- Not checked yetcites [41] Yamaguchi, H. et al. Mutations in TERT, the gene for telomerase reverse transcriptase, in aplastic anemia. N. Engl. J. Med. 352, 1413–1424 (2005). This study identified TERT mutations in patients with aplastic anaemia. source
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In the paper
“In addition to studies in families, a number of population-based twin and non-twin studies have shown that parental telomere length (especially the paternal) influences offspring telomere length with heritability estimates ranging from 0.36–0.84 (reviewed in Ref. 90).”
§ The telomere syndromes > Telomere length is a heritable trait > Heritability of telomere length in humans
What the sources say
- Not checked yetcites [90] Aviv, A. Genetics of leukocyte telomere length and its role in atherosclerosis. Mutat. Res. 730, 68–74 (2012). source
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In the paper
“When quantified, telomere length is short in wild-type offspring of parent M. castaneus mice that have short telomeres, indicating that telomere length is inherited36,82”
- Also stated in: § Evidence from mouse studies · plain
“Therefore, telomere length is inherited as a unique genotype, and its inheritance can be uncoupled from the telomerase and telomere gene loci.”
§ The telomere syndromes > Telomere length is a heritable trait > Evidence from mouse studies
What the sources say
- Not checked yetcites [36] Hao, L. Y. et al. Short telomeres, even in the presence of telomerase, limit tissue renewal capacity. Cell 123, 1121–1131 (2005). In reference 36, using CAST/EiJ mice that have telomere length similar to humans, this paper established that telomerase haploinsufficiency is sufficient to cause dyskeratosis-congenita-like phenotypes. It also showed that telomere length is inherited and can cause degenerative phenotypes even when telomerase is wild-type. source
- Not checked yetcites [82] Armanios, M. et al. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am. J. Hum. Genet. 85, 823–832 (2009). source
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- Also stated in: § Evidence from mouse studies · plain
In the paper
“In earlier generations, pulmonary fibrosis is usually the primary manifestation, whereas in later generations, bone marrow failure in younger individuals is seen as a first complication71.”
§ The telomere syndromes > Genotype–phenotype correlations > Telomere length is a modifier of disease type
What the sources say
- Not checked yetcites [71] Parry, E. M., Alder, J. K., Qi, X., Chen, J. J. & Armanios, M. Syndrome complex of bone marrow failure and pulmonary fibrosis predicts germline defects in telomerase. Blood 117, 5607–5611 (2011). source
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In the paper
“Telomere disorders most commonly manifest as adult-onset disease and as a consequence of germline TERT or TR loss-of-function mutations13.”
§ The telomere syndromes > The monogenic telomere disorders > Adult-onset manifestations of telomere-mediated disease
What the sources say
- Not checked yetcites [13] Armanios, M. Syndromes of telomere shortening. Annu. Rev. Genom. Hum. Genet. 10, 45–61 (2009). source
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In the paper
“The consequent signalling cascades activate checkpoints that induce either cellular senescence or apoptosis, and in at least some contexts both processes occur simultaneously82,85,91,95.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease
What the sources say
- Not checked yetcites [82] Armanios, M. et al. Short telomeres are sufficient to cause the degenerative defects associated with aging. Am. J. Hum. Genet. 85, 823–832 (2009). source
- Not checked yetcites [85] Lee, H. W. et al. Essential role of mouse telomerase in highly proliferative organs. Nature 392, 569–574 (1998). References 84 and 85 are two landmark papers that established that telomerase itself is not essential and that short telomeres cause apoptosis and cell loss in high-turnover tissues. source
- Not checked yetcites [91] d'Adda di Fagagna, F. et al. A DNA damage checkpoint response in telomere-initiated senescence. Nature 426, 194–198 (2003). source
- Not checked yetcites [95] Hemann, M. T. et al. Telomere dysfunction triggers developmentally regulated germ cell apoptosis. Mol. Biol. Cell 12, 2023–2030 (2001). source
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In the paper
“However, the cancer-related mortality is limited to approximately 10% of dyskeratosis congenita cases, with the remaining mortality attributable to the degenerative disease phenotypes described above.”
§ The telomere syndromes > The monogenic telomere disorders > Telomere syndromes predispose to cancer
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In the paper
“The frequency of these mutations is highest in individuals with the progressive disorder IPF, which accounts for 8–15% of familial and 1–3% of sporadic cases54,56,68,69.”
§ The telomere syndromes > The monogenic telomere disorders > Adult-onset manifestations of telomere-mediated disease
What the sources say
- Not checked yetcites [54] Alder, J. K. et al. Short telomeres are a risk factor for idiopathic pulmonary fibrosis. Proc. Natl Acad. Sci. USA 105, 13051–13056 (2008). source
- Not checked yetcites [56] Armanios, M. Y. et al. Telomerase mutations in families with idiopathic pulmonary fibrosis. N. Engl. J. Med. 356, 1317–1326 (2007). References 54–56 showed that lymphocyte telomere length using flow cytometry and fluorescence in situ hybridization could be a useful diagnostic marker in identifying individuals with telomere-related disease. source
- Not checked yetcites [68] Tsakiri, K. D. et al. Adult-onset pulmonary fibrosis caused by mutations in telomerase. Proc. Natl Acad. Sci. USA 104, 7552–7557 (2007). References 56 and 68 identified mutations in the essential telomerase genes in familial pulmonary fibrosis. source
- Not checked yetcites [69] Cronkhite, J.T. et al. Telomere shortening in familial and sporadic pulmonary fibrosis. Am. J. Respir. Crit. Care Med. 178, 729–737 (2008). source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Hence, the degree of telomere shortness is a determinant of both disease severity and type.”
§ The telomere syndromes > Genotype–phenotype correlations > Telomere length is a modifier of disease type
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In the paper
“The downstream effector pathways of telomere-induced senescence are largely p53-dependent96, but there may be involvement of the retinoblastoma protein (RB) pathway in some settings97.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease
What the sources say
- Not checked yetcites [96] Chin, L. et al. p53 deficiency rescues the adverse effects of telomere loss and cooperates with telomere dysfunction to accelerate carcinogenesis. Cell 97, 527–538 (1999). source
- Not checked yetcites [97] Guo, N. et al. Short telomeres compromise β-cell signaling and survival. PLoS ONE 6, e17858 (2011). source
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Eight mutant genes have been identified in dyskeratosis congenita9,38,39,60–64, and all of them encode telomerase or telomere protein components (summarized in Table 1).”
§ The telomere syndromes > The monogenic telomere disorders > Childhood-onset telomere disorders
What the sources say
- Not checked yetcites [9] Heiss, N. S. et al. X-linked dyskeratosis congenita is caused by mutations in a highly conserved gene with putative nucleolar functions. Nature Genet. 19, 32–38 (1998). This study identified mutations in the X-linked DKC1 gene as a first cause of dyskeratosis congenita. source
- Not checked yetcites [38] Vulliamy, T. et al. The RNA component of telomerase is mutated in autosomal dominant dyskeratosis congenita. Nature 413, 432–435 (2001). source
- Not checked yetcites [39] Armanios, M. et al. Haploinsufficiency of telomerase reverse transcriptase leads to anticipation in autosomal dominant dyskeratosis congenita. Proc. Natl Acad. Sci. USA 102, 15960–15964 (2005). References 38 and 39 identified mutations in the essential telomerase genes, TERT and TR , in dyskeratosis congenita. source
- Not checked yetcites [60] Vulliamy, T. et al. Mutations in the telomerase component NHP2 cause the premature ageing syndrome dyskeratosis congenita. Proc. Natl Acad. Sci. USA 105, 8073–8078 (2008). source
- Not checked yetcites [61] Walne, A. J. et al. Genetic heterogeneity in autosomal recessive dyskeratosis congenita with one subtype due to mutations in the telomerase-associated protein NOP10. Hum. Mol. Genet. 16, 1619–1629 (2007). source
- Not checked yetcites [62] Savage, S. A. et al. TINF2, a component of the shelterin telomere protection complex, is mutated in dyskeratosis congenita. Am. J. Hum. Genet. 82, 501–509 (2008). This paper was the first to show that mutations in a shelterin component are a cause of dyskeratosis congenita. source
- Not checked yetcites [63] Zhong, F. et al. Disruption of telomerase trafficking by TCAB1 mutation causes dyskeratosis congenita. Genes Dev. 25, 11–16. source
- Not checked yetcites [64] Keller, R. B. et al. CTC1 mutations in a patient with dyskeratosis congenita. Pediatr. Blood Cancer 59, 311–314 (2012). source
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In the paper
“When examining telomere measurements within a mixed cell population, it is important to note that this is a surrogate marker of the mean in a heterogeneous cell population and that telomere length is mosaic, reflecting the telomere length regulation and replicative history of each cell type51,52.”
§ The telomere syndromes > Telomere length measurement
What the sources say
- Not checked yetcites [51] Lin, J. et al. Analyses and comparisons of telomerase activity and telomere length in human T and B cells: insights for epidemiology of telomere maintenance. J. Immunol. Methods 352, 71–80 (2010). source
- Not checked yetcites [52] Rufer, N. et al. Telomere fluorescence measurements in granulocytes and T lymphocyte subsets point to a high turnover of hematopoietic stem cells and memory T cells in early childhood. J. Exp. Med. 190, 157–167 (1999). source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The limitation on the telomerase synthesis reaction on human telomeres favours telomere shortening as a general default state and means that telomere shortening generally accompanies cell proliferation.”
§ The telomere syndromes > Telomeres and telomerase > Elongation of telomeres by telomerase is tightly regulated
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In the paper
“This idea is consistent with the fact that telomerase activity is upregulated in most human cancers, which probably contributes to sustaining their immortality7.”
§ The telomere syndromes > Telomeres and telomerase > Elongation of telomeres by telomerase is tightly regulated
What the sources say
- Not checked yetcites [7] Kim, N. W. et al. Specific association of human telomerase activity with immortal cells and cancer. Science 266, 2011–2015 (1994). In this study, telomerase activity was found to be enriched in cancer and germ cells, suggesting that telomerase has a role in extending replicative potential. source
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In the paper
“The telomere syndromes are highly relevant for understanding age-related disease because the short telomere defect that they share is acquired with age.”
§ The telomere syndromes > Abstract
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- Rests on an assumption: The short telomere defect shared by telomere syndromes is acquired with age.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The shared underlying telomere defect in aplastic anaemia and IPF brings together clinical entities that were previously considered to be disparate and defines a recognizable syndrome complex that predominantly manifests in adults, in contrast to dyskeratosis congenita.”
§ The telomere syndromes > The monogenic telomere disorders > The telomere syndrome concept
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In the paper
“Telomere elongation is cell-cycle-regulated; telomerase elongates telomeric DNA by adding telomere repeats during S phase and into M phase32,33.”
§ The telomere syndromes > Telomeres and telomerase > Elongation of telomeres by telomerase is tightly regulated
What the sources say
- Not checked yetcites [32] Diede, S. J. & Gottschling, D. E. Telomerase-mediated telomere addition in vivo requires DNA primase and DNA polymerases α and δ. Cell 99, 723–733 (1999). source
- Not checked yetcites [33] Marcand, S., Brevet, V., Mann, C. & Gilson, E. Cell cycle restriction of telomere elongation. Curr. Biol. 10, 487–490 (2000). source
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In the paper
“Indeed, the co-occurrence of IPF and bone marrow failure, along with liver cirrhosis, is specific to and highly predictive of a germline telomere maintenance defect13,39,71.”
§ The telomere syndromes > The monogenic telomere disorders > The telomere syndrome concept
What the sources say
- Not checked yetcites [13] Armanios, M. Syndromes of telomere shortening. Annu. Rev. Genom. Hum. Genet. 10, 45–61 (2009). source
- Not checked yetcites [39] Armanios, M. et al. Haploinsufficiency of telomerase reverse transcriptase leads to anticipation in autosomal dominant dyskeratosis congenita. Proc. Natl Acad. Sci. USA 102, 15960–15964 (2005). References 38 and 39 identified mutations in the essential telomerase genes, TERT and TR , in dyskeratosis congenita. source
- Not checked yetcites [71] Parry, E. M., Alder, J. K., Qi, X., Chen, J. J. & Armanios, M. Syndrome complex of bone marrow failure and pulmonary fibrosis predicts germline defects in telomerase. Blood 117, 5607–5611 (2011). source
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In the paper
“Therefore, it seems that telomere-induced senescence represents more than a loss of replicative potential and can limit cellular function even when cells appear morphologically intact97.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease > Exocytosis defects in pancreatic β-cells
What the sources say
- Not checked yetcites [97] Guo, N. et al. Short telomeres compromise β-cell signaling and survival. PLoS ONE 6, e17858 (2011). source
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Telomere syndromes represent an archetype of premature-ageing syndromes because the short telomere defect they share is progressively acquired with age in humans.”
§ The telomere syndromes > Summary and implications
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Beyond its canonical phenotypes in high-turnover tissues, telomere dysfunction is sufficient to cause — and indeed commonly causes — degenerative phenotypes in slow-turnover tissues.”
§ The telomere syndromes > Summary and implications
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In the paper
“Although they appear morphologically normal, mouse β-cells with dysfunctional telomeres show the hallmarks of senescence. They have an activated DNA damage response, impaired proliferation, p16INK4A upregulation and altered gene expression97.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease > Exocytosis defects in pancreatic β-cells
What the sources say
- Not checked yetcites [97] Guo, N. et al. Short telomeres compromise β-cell signaling and survival. PLoS ONE 6, e17858 (2011). source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The fact that the gene expression changes that occur during telomere-induced senescence cause functional changes in the absence of structural tissue disruption highlights a novel mechanism by which senescence and its associated gene expression changes cause disease.”
§ The telomere syndromes > Mechanisms of telomere-mediated disease > Exocytosis defects in pancreatic β-cells
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The paper relies on this without support.
The short telomere defect shared by telomere syndromes is acquired with age.
“The telomere syndromes are highly relevant for understanding age-related disease because the short telomere defect that they share is acquired with age.”
The paper relies on this without support.
The short telomere defect in affected individuals is present in germ cells and thus simultaneously affects multiple organs even when one disease presentation predominates.
“Their grouping together as a syndrome spectrum is crucial for clinical decisions because the short telomere defect in affected individuals is present in germ cells and thus simultaneously affects multiple organs even when one disease presentation predominates.”
The paper relies on this without support.
Allogeneic stem cell transplantation can reverse aplastic anaemia in humans.
“In humans, the aplastic anaemia phenotype can be reversed with allogeneic stem cell transplant, indicating that this telomere-related stem cell failure state is primarily cell-autonomous.”
The paper relies on this without support.
Smoking hastens disease onset in people who carry telomerase mutations.
“Instead, a second insult is required, and when mice with short telomeres are experimentally exposed to cigarette smoke, which is known to accelerate disease onset in human telomerase mutation carriers, they develop lung disease99.”
The paper relies on this without support.
β-cells in adult mouse pancreatic islets turn over slowly, roughly 4% each week.
“This mechanism has been elucidated in adult mouse β-cells of the pancreatic islets, which have a fairly slow turnover (4% per week).”
The paper relies on this without support.
Blood formation depends on a small set of stem cells that can self-renew and differentiate.
“Haematopoiesis relies on the self-renewal and differentiation capacity of a well-characterized oligoclonal stem cell compartment.”
Claims other papers make about this one
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The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Telomerase deficiency in humans is associated with premature development of diseases, such as pulmonary fibrosis, dyskeratosis congenita and aplastic anemia, which involve the loss of the regenerative capacity of different tissues (Armanios and Blackburn, 2012).”
From The Hallmarks of Aging (2013) · cites this paper as Armanios and Blackburn, 2012
Experimental — accuracy not yet measuredIn the citing paper
“Progerias or premature aging, or the short telomere syndromes include genetic diseases associated with short telomeres and premature senescence [59].”
From Markers of cellular senescence. Telomere shortening as a marker of cellular senescence (2016) · cites this paper as [59]
In the citing paper
“Rare Mendelian human mutations compromising telomere maintenance or protection genes cause early death and diseases involving a wide variety of tissues and organ systems (Armanios and Blackburn, 2012).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Armanios and Blackburn, 2012
In the citing paper
“The ribonucleoprotein enzyme telomerase provides the major mechanism for telomere preservation and length replenishment (Armanios and Blackburn, 2012; Chakhparonian and Wellinger, 2003) (Fig 1).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Armanios and Blackburn, 2012
In the citing paper
“Inherited telomerase deficiencies resulting in a two-fold drop in gene dosage are directly linked to malignancies and several other diseases in humans (Armanios and Blackburn, 2012).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Armanios and Blackburn, 2012
In the citing paper
“Short telomeres have been linked to numerous diseases of aging and in many but not all cases, to all-cause and disease-specific mortality (12–17).”
From Determinants of telomere attrition over 1 year in healthy older women: stress and health behaviors matter (2015) · cites this paper as [12]
In the citing paper
“stress appears to augment replicative TL shortening, perhaps by promoting nonenzymatic hydrolysis of telomere base pairs (11,18).”
From Social disadvantage, genetic sensitivity, and children's telomere length (2014) · cites this paper as [18]
Citations
Cites
Specific Association of Human Telomerase Activity with Immortal Cells and Cancer
Kim, N. W., Piatyszek, M. A., Prowse, K. R., Harley, C. B., West, M. D., Ho, P. L. C., Coviello, G. M., Wright, W. E., Weinrich, S. L., & Shay, J. W. (1994) · Science · doi:10.1126/science.7605428 · Cited by 7,091
Telomeres shorten during ageing of human fibroblasts
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Metadata
- Authors
- Armanios, M., & Blackburn, E. H.
- Affiliations
- Johns Hopkins University (US)
- University of California, San Francisco (US)
- Corresponding author
- Armanios, Mary
- Venue
- Nature Reviews Genetics
- Published
- 2012-09-11
- Volume
- 13
- Issue
- 10
- Pages
- 693-704
- ISSN
- 1471-0056 (ISSN-L)
- 1471-0064
- PMC
- PMC3548426
- OpenAlex
- W1981775109
- Cited by
- 982
- References
- 128
- Citations by year
- 2026: 41 · 2025: 46 · 2024: 50 · 2023: 63 · 2022: 68 · 2021: 92 · 2020: 74 · 2019: 79 · 2018: 81 · 2017: 84 · 2016: 82 · 2015: 80 · 2014: 71 · 2013: 59 · 2012: 8
- FWCI
- 7.50
- Type
- journal article
- Language
- en
- Update notices
- erratum (2013-02-12)
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Nature Reviews Genetics (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R21HL104345)
- National Cancer Institute (R01CA160433)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Structure and Function
- Keywords
- telomere dysfunction, telomere maintenance, short telomeres, cellular aging, idiopathic pulmonary fibrosis, bone marrow failure, degenerative diseases, mode of inheritance, age-related diseases, telomere biology
- MeSH terms
- Animals, Humans, Models, Biological, Syndrome, Telomere, Quantitative Trait, Heritable, Genetic Predisposition to Disease, Genetic Diseases, Inborn, Genetic Association Studies
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