Evidence map›Paper›PMID 25980498›Full record

ArticleOncotarget2015

Pharmacogenomic analysis indicates potential of 1,5-isoquinolinediol as a universal anti-aging agent for different tissues.

Mi Sung Park, Joon-Seok Choi, Wan Lee, Yoon Jung Yang, Juhee Kim, Gun-Joo Lee, Sang Soo Kim, Seong Hoon Park, Sung Chul Kim, Jin Woo Choi

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 8 citations in OpenAlex.

  1. Review
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

10 authors at 2 institutions in 1 country.

Mi Sung ParkInstitute for Metabolic Disease, School of Medicine, Wonkwang University, Iksan, Jeonbuk, South Korea.
Joon-Seok ChoiCollege of Pharmacy, Catholic University of Daegu, Gyeongbuk, South Korea.
Wan LeeDepartment of Oral and Maxillofacial Radiology, College of Dentistry, Wonkwang University, Jeonbuk, South Korea.
Yoon Jung YangWonkwang Institute of Integrative Biomedical Science and Dental Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk, South Korea.
Juhee KimWonkwang Institute of Integrative Biomedical Science and Dental Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk, South Korea.
Gun-Joo LeeWonkwang Institute of Integrative Biomedical Science and Dental Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk, South Korea.
Sang Soo KimJaesaeng Hospital, Biomedical Research Institute, Seongnam, Gyenggi-do, South Korea.
Seong Hoon ParkInstitute for Metabolic Disease, School of Medicine, Wonkwang University, Iksan, Jeonbuk, South Korea.
Sung Chul KimDepartment of Acupuncture and Moxibustion, Wonkwang University Oriental Medical Hospital, Gwangju, South Korea.
Jin Woo ChoiWonkwang Institute of Integrative Biomedical Science and Dental Research Institute, School of Dentistry, Wonkwang University, Iksan, Chonbuk, South Korea.
Wonkwang University · KRAdvanced Institute of Convergence Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The natural aging of multicellular organisms is marked by a progressive decline in the function of cells and tissues. The accumulation of senescent cells in tissues seems to eventually cause aging of the host. Nevertheless, gene expression that influences aging is unlikely to be conserved between tissues, and age-related loss of function seems to depend on a variety of mechanisms. This is a concern when developing anti-aging drugs in geriatric clinical pharmacology. We have sought a universal agent to redundantly cover gene expression despite the variation in differentially expressed genes between tissues. Using a minimally modified connectivity map, the poly (ADP-ribose) polymerase (PARP) inhibitor 1,5-isoquinolinediol was selected as a potent candidate, simultaneously applicable to various tissues. This choice was validated in vitro. Treatment of murine embryonic fibroblasts with 1,5-isoquinolinediol appeared to efficiently suppress the rate of replicative senescence at a concentration of 0.1 µM without resulting in cell death. The appearance of abnormal nuclei and accumulation of β-galactosidase in the cytoplasm were inhibited by daily treatment with the agent. When the aging process was accelerated by hydroxyurea-induced oxidative stress, the effect was even more noticeable. Thus, 1,5-isoquinolinediol may potentially be developed as an agent to prolong life.

Indexed as

AgingAnimalsBlotting, WesternCellular SenescenceGene Expression ProfilingIsoquinolinesMiceMice, Inbred C57BLModels, AnimalPharmacogeneticsPoly(ADP-ribose) Polymerase Inhibitors1,5-dihydroxyisoquinolineIsoquinolinesPoly(ADP-ribose) Polymerase Inhibitorsagingcellular replicative senescencechemical genomicsgene expression profile

Identifiers

PMID25980498
PMCPMC4627305
OpenAlexW1563562242

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.