Evidence map›Paper›PMID 24677687›Full record

ReviewCytometry. Part A : the journal of the International Society for Analytical Cytology2014

In search of antiaging modalities: evaluation of mTOR- and ROS/DNA damage-signaling by cytometry.

Zbigniew Darzynkiewicz, Hong Zhao, H Dorota Halicka, Jiangwei Li, Yong-Syu Lee, Tze-Chen Hsieh, Joseph M Wu

Open access · bronzeAbstract readReview
In one paragraph

Review in Cytometry. Part A : the journal of the International Society for Analytical Cytology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
4.1field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Deciphering the aging process through single-cell cytometric technologies.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2024
    Review
  3. Review
  4. Review
  5. Frontiers in immunology · 2021
    Article
  6. Article
  7. Review
  8. Simultaneous polychromatic flow cytometric detection of multiple forms of regulated cell death.Apoptosis : an international journal on programmed cell death · 2019
    Article
  9. Article
  10. Review
  11. Review
  12. Of Cytometry, Stem Cells and Fountain of Youth.Stem cell reviews and reports · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Zbigniew DarzynkiewiczBrander Cancer Research Institute and Department of Pathology, New York Medical College, Valhalla, New York, 10595.
Hong Zhao
H Dorota Halicka
Jiangwei Li
Yong-Syu Lee
Tze-Chen Hsieh
Joseph M Wu
New York Medical College · USCancer Research Institute · US

Funding

PROBES FOR FLOW CYTOMETRYR01CA028704 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI DARZYNKIEWICZ, ZBIGNIEW · 1985 to 2014
$6.0M
NCI NIH HHS R01 CA028704
6 · The paper itself

Abstract

This review presents the evidence in support of the IGF-1/mTOR/S6K1 signaling as the primary factor contributing to aging and cellular senescence. Reviewed are also specific interactions between mTOR/S6K1 and ROS-DNA damage signaling pathways. Outlined are critical sites along these pathways, including autophagy, as targets for potential antiaging (gero-suppressive) and/or chemopreventive agents. Presented are applications of flow- and laser scanning- cytometry utilizing phospho-specific Abs, to monitor activation along these pathways in response to the reported antiaging drugs rapamycin, metformin, berberine, resveratrol, vitamin D3, 2-deoxyglucose, and acetylsalicylic acid. Specifically, effectiveness of these agents to attenuate the level of constitutive mTOR signaling was tested by cytometry and confirmed by Western blotting through measuring phosphorylation of the mTOR-downstream targets including ribosomal protein S6. The ratiometric analysis of phosphorylated to total protein along the mTOR pathway offers a useful parameter reporting the effects of gero-suppressive agents. In parallel, their ability to suppress the level of constitutive DNA damage signaling induced by endogenous ROS was measured. While the primary target of each of these agents may be different the data obtained on several human cancer cell lines, WI-38 fibroblasts and normal lymphocytes suggest common downstream mechanism in which the decline in mTOR/S6K1 signaling and translation rate is coupled with a reduction of oxidative phosphorylation and ROS that leads to decreased oxidative DNA damage. The combined assessment of constitutive γH2AX expression, mitochondrial activity (ROS, ΔΨm), and mTOR signaling provides an adequate gamut of cell responses to test effectiveness of gero-suppressive agents. Described is also an in vitro model of induction of cellular senescence by persistent replication stress, its quantitative analysis by laser scanning cytometry, and application to detect the property of the studied agents to attenuate the induction of senescence. Discussed is cytometric analysis of cell size and heterogeneity of size as a potential biomarker used to asses gero-suppressive agents and longevity.

Indexed as

AgingAutophagyCellular SenescenceDNA DamageHumansInsulin-Like Growth Factor ILaser Scanning CytometryMitochondriaNuclear ProteinsPhosphorylationReactive Oxygen SpeciesRNA-Binding ProteinsSignal TransductionTOR Serine-Threonine KinasesInsulin-Like Growth Factor IMTOR protein, humanNuclear ProteinsPOLDIP3 protein, humanReactive Oxygen SpeciesRNA-Binding ProteinsTOR Serine-Threonine Kinasesberberinecell sizecellular senescenceDNA damage signalingH2AX phosphorylationmitochondriared cell distribution widthreplication stressribosomal protein S6 phosphorylationtranslation

Identifiers

PMID24677687
PMCPMC4080725
OpenAlexW2169651072

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.