Evidence map›Paper›PMID 32194054›Full record

ReviewThe American journal of pathology2020

Chronic Kidney Disease: A Vicarious Relation to Premature Cell Senescence.

Michael S Goligorsky

Open access · bronzeAbstract readReview
In one paragraph

Review in The American journal of pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.2field-weighted citation impact, top 5% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Chronic Kidney Disease and Cellular Senescence.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Protective Role of Serum β-Hydroxybutyrate in Early Diabetic Kidney Disease: A Longitudinal Study.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2025
    Article
  4. Review
  5. Review
  6. Transglutaminase 2-mediated glutamine deamidation enhances p21 stability during senescence.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Permissive role of vascular endothelium in fibrosis: focus on the kidney.American journal of physiology. Cell physiology · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Review
  19. Klotho, Aging, and the Failing Kidney.Frontiers in endocrinology · 2020
    Review
  20. 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

1 author at 1 institution in 1 country.

Michael S GoligorskyRenal Research Institute, and the Departments of Medicine, Pharmacology, and Physiology, New York Medical College at Touro University, Valhalla, New York. Electronic address: michael_goligorsky@nymc.edu.
New York Medical College · US

Funding

Glycocalyx repair in sepsis using liposomal carriers of preassembled glycocalyxR01HL144528 · NHLBI · NEW YORK MEDICAL COLLEGE · PI GOLIGORSKY, MICHAEL S, SUN, DONG · 2019 to 2022
$2.2M
NHLBI NIH HHS R01 HL144528
6 · The paper itself

Abstract

Chronic kidney disease (CKD), commonly fostering nonrenal complications, themselves more life threatening than renal pathology, remains enigmatic. Despite more than a century of intense research, therapeutic options to halt or reverse renal disease are rather limited. Recently, similarity between manifestations of progressive CKD and aging kidney has attracted investigative attention that revealed senescent cells and secreting proinflammatory and profibrotic mediators in all renal compartments, even at young age, in patients with kidney maladies. The overlapping features of these categories have been noticed previously and are briefly summarized herein. I propose two hypothetical scenarios for interactive association of kidney diseases and cell senescence, both culminating in progressive deterioration of renal function. Persistence of senescent cells is considered as a critical contributor to this association; and the mechanisms explaining persistence, such as activation of cell cycle regulators, anti-apoptotic stimuli, metabolic aberrations, and their interactions, are discussed. The mutual encroachment of underlying kidney disease and cell senescence bring about the conclusion that both entities merge along the natural history of the disease. This putative interpretation of vicarious relation between cell senescence and CKD may expand the arsenal of pharmacotherapy to include the judicious use of senotherapeutics in the management of renal disease.

Indexed as

Cellular SenescenceHumansKidneyRenal Insufficiency, Chronic

Identifiers

PMID32194054
PMCPMC7280755
OpenAlexW3010704565

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.