Evidence map›Paper›PMID 38107570›Full record

ArticlePeerJ2023

Exploring the anti-aging effects of fisetin in telomerase-deficient progeria mouse model.

Rui Zhao, Haomeng Kou, Duo Jiang, Feng Wang

Open access · goldAbstract read
In one paragraph

Article in PeerJ, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Review
  3. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. 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

4 authors at 1 institution in 1 country.

Rui Zhao *Department of Genetics, Tianjin Medical University, Tianjin, China.
Haomeng Kou *Department of Genetics, Tianjin Medical University, Tianjin, China.
Duo JiangDepartment of Genetics, Tianjin Medical University, Tianjin, China.
Feng WangDepartment of Genetics, Tianjin Medical University, Tianjin, China.
Tianjin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aging is a natural and complex process characterized by the gradual deterioration of tissue and physiological functions in the organism over time. Cell senescence, a hallmark of aging, refers to the permanent and irreversible cell cycle arrest of proliferating cells triggered by endogenous stimuli or environmental stresses. Eliminating senescent cells has been shown to extend the healthy lifespan. In this study, we established a progeria mouse model with telomerase deficiency and confirmed the presence of shortened telomere length and increased expression of aging markers

Indexed as

ProgeriaTelomeraseAgingAnimalsCyclin-Dependent Kinase Inhibitor p16FlavonolsMiceProto-Oncogene Proteins c-aktTelomereTelomere ShorteningCyclin-Dependent Kinase Inhibitor p16fisetinFlavonolsProto-Oncogene Proteins c-aktTelomeraseAgingFisetinSenolyticsTelomerase deficient

Identifiers

PMID38107570
PMCPMC10722989
OpenAlexW4389623022

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.