Evidence map›Paper›PMID 29260442›Full record

ReviewJournal of cell communication and signaling2018

Cellular senescence in the aging and diseased kidney.

F A Valentijn, L L Falke, T Q Nguyen, Roel Goldschmeding

Open access · hybridAbstract readReview
In one paragraph

Review in Journal of cell communication and signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
106citing papers in PubMed, 1 pooled it
7.8field-weighted citation impact, top 2% 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

106 citing papers in PubMed, 1 synthesis or guideline pooled it, 163 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Downregulation of EZH2 Promotes Renal Epithelial Cellular Senescence and Kidney Aging.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

46 more citing papers are in PubMed but not listed here.

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 2 countries.

F A ValentijnDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 110, 3584, CX, Utrecht, The Netherlands.
L L FalkeDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 110, 3584, CX, Utrecht, The Netherlands.
T Q NguyenDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 110, 3584, CX, Utrecht, The Netherlands.
Roel GoldschmedingDepartment of Pathology, University Medical Center Utrecht, H04.312, Heidelberglaan 110, 3584, CX, Utrecht, The Netherlands. R.Goldschmeding@umcutrecht.nl.ORCID http://orcid.org/0000-0002-5471-1153
Heidelberg University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The program of cellular senescence is involved in both the G1 and G2 phase of the cell cycle, limiting G1/S and G2/M progression respectively, and resulting in prolonged cell cycle arrest. Cellular senescence is involved in normal wound healing. However, multiple organs display increased senescent cell numbers both during natural aging and after injury, suggesting that senescent cells can have beneficial as well as detrimental effects in organismal aging and disease. Also in the kidney, senescent cells accumulate in various compartments with advancing age and renal disease. In experimental studies, forced apoptosis induction through the clearance of senescent cells leads to better preservation of kidney function during aging. Recent groundbreaking studies demonstrate that senescent cell depletion through INK-ATTAC transgene-mediated or cell-penetrating FOXO4-DRI peptide induced forced apoptosis, reduced age-associated damage and dysfunction in multiple organs, in particular the kidney, and increased performance and lifespan. Senescence is also involved in oncology and therapeutic depletion of senescent cells by senolytic drugs has been studied in experimental and human cancers. Although studies with senolytic drugs in models of kidney injury are lacking, their dose limiting side effects on other organs suggest that targeted delivery might be needed for successful application of senolytic drugs for treatment of kidney disease. In this review, we discuss (i) current understanding of the mechanisms and associated pathways of senescence, (ii) evidence of senescence occurrence and causality with organ injury, and (iii) therapeutic strategies for senescence depletion (senotherapy) including targeting, all in the context of renal aging and disease.

Indexed as

Apoptotic balanceCellular senescenceDNA damage responseRenal agingRenal diseaseSenotherapy

Identifiers

PMID29260442
PMCPMC5842195
OpenAlexW2780553069

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.