Evidence map›Paper›PMID 32592814›Full record

ArticleKidney international2020

Global transcriptomic changes occur in aged mouse podocytes.

Yuliang Wang, Diana G Eng, Natalya V Kaverina, Carol J Loretz, Abbal Koirala, Shreeram Akilesh, Jeffrey W Pippin, Stuart J Shankland

Abstract read
In one paragraph

Article in Kidney international, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed.

  1. Alterations of actin in aging.Journal of cell science · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  7. Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. LRG1 loss effectively restrains glomerular TGF-β signaling to attenuate diabetic kidney disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  16. Gene regulatory networks in disease and ageing.Nature reviews. Nephrology · 2024
    Review
  17. Article
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Yuliang WangPaul G. Allen School of Computer Science and Engineering, University of Washington, Seattle, Washington, USA; Institute for Stem Cell & Regenerative Medicine, University of Washington, Seattle, Washington, USA.
Diana G EngDivision of Nephrology, University of Washington, Seattle, Washington, USA.
Natalya V KaverinaDivision of Nephrology, University of Washington, Seattle, Washington, USA.
Carol J LoretzDivision of Nephrology, University of Washington, Seattle, Washington, USA.
Abbal KoiralaDivision of Nephrology, University of Washington, Seattle, Washington, USA.
Shreeram AkileshDepartment of Pathology, University of Washington, Seattle, Washington, USA.
Jeffrey W PippinDivision of Nephrology, University of Washington, Seattle, Washington, USA.
Stuart J ShanklandDivision of Nephrology, University of Washington, Seattle, Washington, USA. Electronic address: stuartjs@uw.edu.

Funding

Juxta-glomerular cells serve as glomerular epithelial cell progenitors in glomerular diseaseR01DK097598 · NIDDK · UNIVERSITY OF WASHINGTON · PI SHANKLAND, STUART JAMES, WESSELY, OLIVER · 2014 to 2022
$5.2M
CELL CYCLE PROTEINS AND GLOMERULAR APOPTOSISR01DK056799 · NIDDK · UNIVERSITY OF WASHINGTON · PI SHANKLAND, STUART JAMES · 2000 to 2014
$3.6M
NIDDK NIH HHS R01 DK056799NIDDK NIH HHS R01 DK097598
6 · The paper itself

Abstract

Glomerular podocytes undergo structural and functional changes with advanced age, that increase susceptibility of aging kidneys to worse outcomes following superimposed glomerular diseases. To delineate transcriptional changes in podocytes in aged mice, RNA-seq was performed on isolated populations of reporter-labeled (tdTomato) podocytes from multiple young (two to three months) and advanced aged mice (22 to 24 months, equivalent to 70 plus year old humans). Of the 2,494 differentially expressed genes, 1,219 were higher and 1,275 were lower in aged podocytes. Pathway enrichment showed that major biological processes increased in aged podocytes included immune responses, non-coding RNA metabolism, gene silencing and MAP kinase signaling. Conversely, aged podocytes showed downregulation of developmental, morphogenesis and metabolic processes. Canonical podocyte marker gene expression decreased in aged podocytes, with increases in apoptotic and senescence genes providing a mechanism for the progressive loss of podocytes seen with aging. In addition, we revealed aberrations in the podocyte autocrine signaling network, identified the top transcription factors perturbed in aged podocytes, and uncovered candidate gene modulations that might promote healthy aging in podocytes. The transcriptional signature of aging is distinct from other kidney diseases. Thus, our study provides insights into biomarker discovery and molecular targeting of the aging process itself within podocytes.

Indexed as

PodocytesAgingAnimalsKidney GlomerulusMiceSignal TransductionTranscriptomeagingdifferentially expressed genesgene ontologyglomeruluspodocyteRNA sequencing

Identifiers

PMID32592814
PMCPMC7606654

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Registered trials

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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.