Evidence map›Paper›PMID 28029153›Full record

ReviewNature reviews. Nephrology2017

Cellular senescence in renal ageing and disease.

Ines Sturmlechner, Matej Durik, Cynthia J Sieben, Darren J Baker, Jan M van Deursen

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 211 papers.

0numbers the graph read from it
0cells of the map it votes in
211citing papers in PubMed
–field-weighted citation impact
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

211 citing papers in PubMed.

  1. Article
  2. Review
  3. Magnesium Attenuates Renal Senescence and Fibrosis With Reduced DNA Damage Response and H3K4me3 Enrichment at the p16FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Deciphering the impact ofGenes & diseases · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  16. Review
  17. Article
  18. Kidney Disease as a Driver of Immunosenescence: Mechanisms and Potential Interventions.Journal of the American Society of Nephrology : JASN · 2026
    Review
  19. Telomere Dysfunction in Renal Tubular Epithelial Cells Leads to Kidney Fibrosis.Journal of the American Society of Nephrology : JASN · 2025
    Article
  20. Article

151 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

5 authors.

Ines SturmlechnerDepartments of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, USA.
Matej DurikDepartments of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, USA.
Cynthia J SiebenDepartment of Biochemistry and Molecular Biology, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, USA.
Darren J BakerDepartments of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, USA.
Jan M van DeursenDepartments of Pediatric and Adolescent Medicine, Mayo Clinic, 200 First Street SW, Rochester, Minnesota, 55905, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The senescence programme is implicated in diverse biological processes, including embryogenesis, tissue regeneration and repair, tumorigenesis, and ageing. Although in vivo studies of senescence are in their infancy, evidence suggesting that senescent cells are a heterogeneous cell type is accumulating: senescence can be induced by different stressors, and senescent cells have varying degrees of genomic and epigenomic instability and different cell origins, contributing to their diversity. Two main classes of senescent cells have been identified: acute and chronic senescent cells. Acute senescent cells are generated during coordinated, beneficial biological processes characterized by a defined senescence trigger, transient senescent-cell signalling functions, and eventual senescent-cell clearance. In contrast, chronic senescent cells arise more slowly from cumulative, diverse stresses and are inefficiently eliminated, leading to their accumulation and deleterious effects through a secretory phenotype. Senescent cells have been identified in many tissues and organs, including the kidney. Here, we discuss the emerging roles of senescent cells in renal development, homeostasis, and pathology. We also address how senotherapy, or targeting of senescent cells, might be used to improve renal function with normal ageing, disease, or therapy-induced damage.

Indexed as

Cellular SenescenceAgingAnimalsHumansKidneyKidney Diseases

Identifiers

What OpenQuestion holds

Textmetadata
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.