Telomerase and mammalian ageing: a critical appraisal

Goyns, M.H.; Lavery, W. Lindsay

doi:10.1016/s0047-6374(00)00095-6

Cited by 46 publications

(22 citation statements)

References 56 publications

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“…Cells that do proliferate frequently have been shown to have active telomerase, and reintroduction of telomerase can prevent the onset of scheduled cellular senescence. However, there is no correlation between telomere length and the maximal life span exhibited by di¡erent species [45]. The mechanism by which a short telomere induces the senescent phenotype is unknown.…”

Section: Discussionmentioning

confidence: 99%

Hutchinson-Gilford Progeria Syndrome: A Pathologic Study

Ackerman

Gilbert‐Barness

2002

Pediatric Pathology & Molecular Medicine

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Hutchinson-Gilford progeria syndrome is an extremely rare condition with features of premature and accelerated aging.The pattern of inheritance is unclear, although both autosomal recessive and autosomal dominant modes have been proposed. The children usually present in late infancy and early childhood with a characteristic phenotype of alopecia; short stature; abnormal skin, teeth, and nails; beaked nose; loss of subcutaneous fat; and failure to thrive.This condition has been reported on all inhabited continents and has been described in all major races. Laboratory ¢ndings note an increased urinary excretion of hyaluronic acid. Death results from cardiovascular abnormalities in the majority of cases and usually occurs in the second decade of life. There is no e¡ective treatment.We report the pathologic changes noted at autopsy on a 20-year-old woman with classic features of Hutchinson-Gilford progeria syndrome.

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Section: Discussionmentioning

confidence: 99%

Hutchinson-Gilford Progeria Syndrome: A Pathologic Study

Ackerman

Gilbert‐Barness

2002

Pediatric Pathology & Molecular Medicine

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“…It is more likely that the same mechanism(s) by which mutant LMNA produces accelerated aging in tissues, such as replicative senescence, 52 telomere shortening, 53 decreased capacity to propogate in subculture, 54 and decreased repair capacity, 55 may also affect vascular wall components. For instance, endothelial cells with mutant LMNA might not regenerate fully to restore intimal integrity after injury.…”

Section: Atherosclerosis In Hgpsmentioning

confidence: 99%

Laminopathies and Atherosclerosis

Alshali

Hegele

2004

ATVB

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Abstract-Laminopathies are genetic diseases that encompass a wide spectrum of phenotypes with diverse tissue pathologies and result mainly from mutations in the LMNA gene encoding nuclear lamin A/C. Some laminopathies affect the cardiovascular system, and a few (namely, Dunnigan-type familial partial lipodystrophy [FPLD2] and HutchinsonGilford progeria syndrome [HGPS]) feature atherosclerosis as a key component. The premature atherosclerosis of FPLD2 is probably related to characteristic proatherogenic metabolic disturbances such as dyslipidemia, hyperinsulinemia, hypertension, and diabetes. In contrast, the premature atherosclerosis of HGPS occurs with less exposure to metabolic proatherogenic traits and probably reflects the generalized process of accelerated aging in HGPS. Although some common polymorphisms of LMNA have been associated with traits related to atherosclerosis, the monogenic diseases Key Words: nuclear envelope Ⅲ insulin resistance Ⅲ aging Ⅲ vascular disease Ⅲ progeria T he nuclear lamina is a 20-nm filamentous meshwork that underlies the inner nuclear membrane and plays a central role in defining interphase nuclear architecture, DNA replication, and chromatin organization. 1 Nuclear lamins are type V intermediate filaments that are the major components of the nuclear lamina.

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“…These telomeres' lengths are maintained by the activity of the enzyme, telomerase, and are thought to be important protective factors in maintaining the integrity of chromosomes 19. It now appears that in vitro replicative senescence, which has been observed in cultured somatic cells, is caused by a loss of telomere length in those cells, caused by inactivity of telomerase 19…”

Section: Laboratory Biochemical and Cellular Abnormalitiesmentioning

confidence: 99%