Evidence map›Paper›PMID 25664244›Full record

ReviewWorld journal of nephrology2015

Aging and uremia: Is there cellular and molecular crossover?

William E White, Muhammad M Yaqoob, Steven M Harwood

Open access · bronzeAbstract readReview
In one paragraph

Review in World journal of nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-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

18 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Premature Aging in Chronic Kidney Disease: The Outcome of Persistent Inflammation beyond the Bounds.International journal of environmental research and public health · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Co-Expression Analysis of Blood Cell Genome Expression to Preliminary Investigation of Regulatory Mechanisms in Uremia.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  18. Article
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

3 authors at 1 institution in 2 countries.

William E WhiteWilliam E White, Muhammad M Yaqoob, Steven M Harwood, Queen Mary University of London, Translational Medicine and Therapeutics, William Harvey Research Institute, John Vane Science Centre, EC1M 6BQ London, United Kingdom.
Muhammad M YaqoobWilliam E White, Muhammad M Yaqoob, Steven M Harwood, Queen Mary University of London, Translational Medicine and Therapeutics, William Harvey Research Institute, John Vane Science Centre, EC1M 6BQ London, United Kingdom.
Steven M HarwoodWilliam E White, Muhammad M Yaqoob, Steven M Harwood, Queen Mary University of London, Translational Medicine and Therapeutics, William Harvey Research Institute, John Vane Science Centre, EC1M 6BQ London, United Kingdom.
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many observers have noted that the morphological changes that occur in chronic kidney disease (CKD) patients resemble those seen in the geriatric population, with strikingly similar morbidity and mortality profiles and rates of frailty in the two groups, and shared characteristics at a pathophysiological level especially in respect to the changes seen in their vascular and immune systems. However, whilst much has been documented about the shared physical characteristics of aging and uremia, the molecular and cellular similarities between the two have received less attention. In order to bridge this perceived gap we have reviewed published research concerning the common molecular processes seen in aging subjects and CKD patients, with specific attention to altered proteostasis, mitochondrial dysfunction, post-translational protein modification, and senescence and telomere attrition. We have also sought to illustrate how the cell death and survival pathways apoptosis, necroptosis and autophagy are closely interrelated, and how an understanding of these overlapping pathways is helpful in order to appreciate the shared molecular basis behind the pathophysiology of aging and uremia. This analysis revealed many common molecular characteristics and showed similar patterns of cellular dysfunction. We conclude that the accelerated aging seen in patients with CKD is underpinned at the molecular level, and that a greater understanding of these molecular processes might eventually lead to new much needed therapeutic strategies of benefit to patients with renal disease.

Indexed as

AgingApoptosisAutophagyKlothoMitochondriaPost-translational protein modificationSenescenceTelomeresUremia

Identifiers

PMID25664244
PMCPMC4317625
OpenAlexW2332425387

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.