Control of cell proliferation in senescent cells

H. R. Warner, J. Campisi, V. J. Cristofalo, R. A. Miller, John Papaconstantinou, O. Pereira-Smith, J. R. Smith, E. Wang

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

The discussions described briefly above have provided an agenda for research on aging at the molecular and cellular level for several years to come. Of central importance is the need to distinguish, at the cellular level, aging from terminal differentiation and disease. Are there terminal differentiation functions that we misinterpret as aging? Are there regulatory pathways of aging? Is cell senescence a true opposite of tumorigenesis? What exactly is the G1/S block? Why are most but not all G1 genes expressed in senescent cells? What roles do changes in RNA processing and protein synthesis play in cell senescence? How is down-regulation of tissue-specific genes effected? These are the critical questions at the cellular level. Of equal importance is the need to establish correspondence between cell senescence phenomena and organismal aging. The similarities between cells aged in culture and cells aged in vivo are encouraging, but cell senescence in culture is neither the ideal nor the only model system for studying aging. Continued and expanded efforts to study aging in vivo in a variety of animal models are clearly needed. Finally, of utmost importance is the need to elucidate how caloric restriction slows the rate of aging and retards the onset of age-related disease. Although this is a whole body phenomenon, it seems likely that understanding how this works will shed considerable light not only on aging but on tumorigenesis as well.

Original languageEnglish (US)
JournalJournals of Gerontology
Volume47
Issue number6
StatePublished - 1992
Externally publishedYes

Fingerprint

Cell Aging
Cell Proliferation
Carcinogenesis
Caloric Restriction
Age of Onset
Genes
Down-Regulation
Animal Models
Cell Culture Techniques
RNA
Research
Proteins

ASJC Scopus subject areas

  • Aging

Cite this

Warner, H. R., Campisi, J., Cristofalo, V. J., Miller, R. A., Papaconstantinou, J., Pereira-Smith, O., ... Wang, E. (1992). Control of cell proliferation in senescent cells. Journals of Gerontology, 47(6).

Control of cell proliferation in senescent cells. / Warner, H. R.; Campisi, J.; Cristofalo, V. J.; Miller, R. A.; Papaconstantinou, John; Pereira-Smith, O.; Smith, J. R.; Wang, E.

In: Journals of Gerontology, Vol. 47, No. 6, 1992.

Research output: Contribution to journalArticle

Warner, HR, Campisi, J, Cristofalo, VJ, Miller, RA, Papaconstantinou, J, Pereira-Smith, O, Smith, JR & Wang, E 1992, 'Control of cell proliferation in senescent cells', Journals of Gerontology, vol. 47, no. 6.
Warner HR, Campisi J, Cristofalo VJ, Miller RA, Papaconstantinou J, Pereira-Smith O et al. Control of cell proliferation in senescent cells. Journals of Gerontology. 1992;47(6).
Warner, H. R. ; Campisi, J. ; Cristofalo, V. J. ; Miller, R. A. ; Papaconstantinou, John ; Pereira-Smith, O. ; Smith, J. R. ; Wang, E. / Control of cell proliferation in senescent cells. In: Journals of Gerontology. 1992 ; Vol. 47, No. 6.
@article{c28eb0861afc43a080287c11c8a55237,
title = "Control of cell proliferation in senescent cells",
abstract = "The discussions described briefly above have provided an agenda for research on aging at the molecular and cellular level for several years to come. Of central importance is the need to distinguish, at the cellular level, aging from terminal differentiation and disease. Are there terminal differentiation functions that we misinterpret as aging? Are there regulatory pathways of aging? Is cell senescence a true opposite of tumorigenesis? What exactly is the G1/S block? Why are most but not all G1 genes expressed in senescent cells? What roles do changes in RNA processing and protein synthesis play in cell senescence? How is down-regulation of tissue-specific genes effected? These are the critical questions at the cellular level. Of equal importance is the need to establish correspondence between cell senescence phenomena and organismal aging. The similarities between cells aged in culture and cells aged in vivo are encouraging, but cell senescence in culture is neither the ideal nor the only model system for studying aging. Continued and expanded efforts to study aging in vivo in a variety of animal models are clearly needed. Finally, of utmost importance is the need to elucidate how caloric restriction slows the rate of aging and retards the onset of age-related disease. Although this is a whole body phenomenon, it seems likely that understanding how this works will shed considerable light not only on aging but on tumorigenesis as well.",
author = "Warner, {H. R.} and J. Campisi and Cristofalo, {V. J.} and Miller, {R. A.} and John Papaconstantinou and O. Pereira-Smith and Smith, {J. R.} and E. Wang",
year = "1992",
language = "English (US)",
volume = "47",
journal = "Journal of Gerontology: Social Sciences",
issn = "0022-1422",
publisher = "Gerontological Society of America",
number = "6",

}

TY - JOUR

T1 - Control of cell proliferation in senescent cells

AU - Warner, H. R.

AU - Campisi, J.

AU - Cristofalo, V. J.

AU - Miller, R. A.

AU - Papaconstantinou, John

AU - Pereira-Smith, O.

AU - Smith, J. R.

AU - Wang, E.

PY - 1992

Y1 - 1992

N2 - The discussions described briefly above have provided an agenda for research on aging at the molecular and cellular level for several years to come. Of central importance is the need to distinguish, at the cellular level, aging from terminal differentiation and disease. Are there terminal differentiation functions that we misinterpret as aging? Are there regulatory pathways of aging? Is cell senescence a true opposite of tumorigenesis? What exactly is the G1/S block? Why are most but not all G1 genes expressed in senescent cells? What roles do changes in RNA processing and protein synthesis play in cell senescence? How is down-regulation of tissue-specific genes effected? These are the critical questions at the cellular level. Of equal importance is the need to establish correspondence between cell senescence phenomena and organismal aging. The similarities between cells aged in culture and cells aged in vivo are encouraging, but cell senescence in culture is neither the ideal nor the only model system for studying aging. Continued and expanded efforts to study aging in vivo in a variety of animal models are clearly needed. Finally, of utmost importance is the need to elucidate how caloric restriction slows the rate of aging and retards the onset of age-related disease. Although this is a whole body phenomenon, it seems likely that understanding how this works will shed considerable light not only on aging but on tumorigenesis as well.

AB - The discussions described briefly above have provided an agenda for research on aging at the molecular and cellular level for several years to come. Of central importance is the need to distinguish, at the cellular level, aging from terminal differentiation and disease. Are there terminal differentiation functions that we misinterpret as aging? Are there regulatory pathways of aging? Is cell senescence a true opposite of tumorigenesis? What exactly is the G1/S block? Why are most but not all G1 genes expressed in senescent cells? What roles do changes in RNA processing and protein synthesis play in cell senescence? How is down-regulation of tissue-specific genes effected? These are the critical questions at the cellular level. Of equal importance is the need to establish correspondence between cell senescence phenomena and organismal aging. The similarities between cells aged in culture and cells aged in vivo are encouraging, but cell senescence in culture is neither the ideal nor the only model system for studying aging. Continued and expanded efforts to study aging in vivo in a variety of animal models are clearly needed. Finally, of utmost importance is the need to elucidate how caloric restriction slows the rate of aging and retards the onset of age-related disease. Although this is a whole body phenomenon, it seems likely that understanding how this works will shed considerable light not only on aging but on tumorigenesis as well.

UR - http://www.scopus.com/inward/record.url?scp=0026566965&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026566965&partnerID=8YFLogxK

M3 - Article

C2 - 1430846

AN - SCOPUS:0026566965

VL - 47

JO - Journal of Gerontology: Social Sciences

JF - Journal of Gerontology: Social Sciences

SN - 0022-1422

IS - 6

ER -