Therapeutic interventions for aging: The case of cellular senescence

Abel Soto-Gamez; Marco Demaria

doi:10.1016/j.drudis.2017.01.004

Therapeutic interventions for aging: The case of cellular senescence

Abel Soto-Gamez, Marco Demaria^*

^*Corresponding author for this work

Research output: Contribution to journal › Review article › peer-review

137 Citations (Scopus)

636 Downloads (Pure)

Abstract

Organismal aging is a multifactorial process characterized by the onset of degenerative conditions and cancer. One of the key drivers of aging is cellular senescence, a state of irreversible growth arrest induced by many pro-tumorigenic stresses. Senescent cells accumulate late in life and at sites of age-related pathologies, where they contribute to disease onset and progression through complex cell and non-cell autonomous effects. Here, we summarize the mechanisms by which cellular senescence can promote aging, and we offer an extensive description of current potential pharmacological interventions for senescent cells, highlighting limitations and suggesting alternatives.

Original language	English
Pages (from-to)	786-795
Number of pages	10
Journal	Drug Discovery Today
Volume	22
Issue number	5
DOIs	https://doi.org/10.1016/j.drudis.2017.01.004
Publication status	Published - May-2017

Keywords

DNA-DAMAGE RESPONSE
NF-KAPPA-B
PLASMINOGEN-ACTIVATOR INHIBITOR-1
MESENCHYMAL STEM-CELLS
SECRETORY PHENOTYPE
CANCER-THERAPY
LIFE-SPAN
IN-VIVO
HUMAN FIBROBLASTS
NKG2D RECEPTOR

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title = "Therapeutic interventions for aging: The case of cellular senescence",

abstract = "Organismal aging is a multifactorial process characterized by the onset of degenerative conditions and cancer. One of the key drivers of aging is cellular senescence, a state of irreversible growth arrest induced by many pro-tumorigenic stresses. Senescent cells accumulate late in life and at sites of age-related pathologies, where they contribute to disease onset and progression through complex cell and non-cell autonomous effects. Here, we summarize the mechanisms by which cellular senescence can promote aging, and we offer an extensive description of current potential pharmacological interventions for senescent cells, highlighting limitations and suggesting alternatives.",

keywords = "DNA-DAMAGE RESPONSE, NF-KAPPA-B, PLASMINOGEN-ACTIVATOR INHIBITOR-1, MESENCHYMAL STEM-CELLS, SECRETORY PHENOTYPE, CANCER-THERAPY, LIFE-SPAN, IN-VIVO, HUMAN FIBROBLASTS, NKG2D RECEPTOR",

author = "Abel Soto-Gamez and Marco Demaria",

year = "2017",

month = may,

doi = "10.1016/j.drudis.2017.01.004",

language = "English",

volume = "22",

pages = "786--795",

journal = "Drug Discovery Today",

issn = "1359-6446",

publisher = "ELSEVIER SCI LTD",

number = "5",

}

TY - JOUR

T1 - Therapeutic interventions for aging

T2 - The case of cellular senescence

AU - Soto-Gamez, Abel

AU - Demaria, Marco

PY - 2017/5

Y1 - 2017/5

N2 - Organismal aging is a multifactorial process characterized by the onset of degenerative conditions and cancer. One of the key drivers of aging is cellular senescence, a state of irreversible growth arrest induced by many pro-tumorigenic stresses. Senescent cells accumulate late in life and at sites of age-related pathologies, where they contribute to disease onset and progression through complex cell and non-cell autonomous effects. Here, we summarize the mechanisms by which cellular senescence can promote aging, and we offer an extensive description of current potential pharmacological interventions for senescent cells, highlighting limitations and suggesting alternatives.

AB - Organismal aging is a multifactorial process characterized by the onset of degenerative conditions and cancer. One of the key drivers of aging is cellular senescence, a state of irreversible growth arrest induced by many pro-tumorigenic stresses. Senescent cells accumulate late in life and at sites of age-related pathologies, where they contribute to disease onset and progression through complex cell and non-cell autonomous effects. Here, we summarize the mechanisms by which cellular senescence can promote aging, and we offer an extensive description of current potential pharmacological interventions for senescent cells, highlighting limitations and suggesting alternatives.

KW - DNA-DAMAGE RESPONSE

KW - NF-KAPPA-B

KW - PLASMINOGEN-ACTIVATOR INHIBITOR-1

KW - MESENCHYMAL STEM-CELLS

KW - SECRETORY PHENOTYPE

KW - CANCER-THERAPY

KW - LIFE-SPAN

KW - IN-VIVO

KW - HUMAN FIBROBLASTS

KW - NKG2D RECEPTOR

U2 - 10.1016/j.drudis.2017.01.004

DO - 10.1016/j.drudis.2017.01.004

M3 - Review article

C2 - 28111332

SN - 1359-6446

VL - 22

SP - 786

EP - 795

JO - Drug Discovery Today

JF - Drug Discovery Today

IS - 5

ER -

Therapeutic interventions for aging: The case of cellular senescence

Abstract

Keywords

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