Evidence map›Paper›PMID 17901943›Full record

ArticleDiabetologia2007

Increased glomerular cell (podocyte) apoptosis in rats with streptozotocin-induced diabetes mellitus: role in the development of diabetic glomerular disease.

S Menini, C Iacobini, G Oddi, C Ricci, P Simonelli, S Fallucca, M Grattarola, F Pugliese, C Pesce, G Pugliese

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In one paragraph

Article in Diabetologia, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
  2. Histone modification in podocyte injury of diabetic nephropathy.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The role of sirolimus in proteinuria in diabetic nephropathy rats.Iranian journal of basic medical sciences · 2017
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Sirtuin 1: A Target for Kidney Diseases.Molecular medicine (Cambridge, Mass.) · 2015
    Review
  13. Review
  14. Enhanced epithelial-to-mesenchymal transition associated with lysosome dysfunction in podocytes: role of p62/Sequestosome 1 as a signaling hub.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2015
    Article
  15. Article
  16. Mycophenolate mofetil inhibits hypertrophy and apoptosis of podocyte in vivo and in vitro.International journal of clinical and experimental medicine · 2015
    Article
  17. Review
  18. Article
  19. Article
  20. 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

10 authors at 1 institution in 1 country.

S MeniniDepartment of Clinical Sciences, La Sapienza University, Viale del Policlinico, 155-00161, Rome, Italy.
C Iacobini
G Oddi
C Ricci
P Simonelli
S Fallucca
M Grattarola
F Pugliese
C Pesce
G Pugliese
University of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisPodocyte loss by apoptosis, in addition to favouring progression of established diabetic nephropathy, has been recently indicated as an early phenomenon triggering the initiation of glomerular lesions. This study aimed to assess the rate of glomerular cell death and its relationship with renal functional, structural and molecular changes in rats with experimental diabetes.

methodsMale Sprague-Dawley rats with streptozotocin-induced diabetes and coeval non-diabetic control animals were killed at 7 days and at 2, 4 and 6 months for the assessment of apoptosis, renal function, renal structure and the expression of podocyte markers and apoptosis- and cell cycle-related proteins.

resultsGlomerular cell apoptosis was significantly increased in diabetic vs non-diabetic rats at 4 months and to an even greater extent at 6 months, with podocytes accounting for 70% of apoptosing cells. The increase in apoptosis was preceded by increases in proteinuria, albuminuria and mean glomerular and mesangial areas, and by reductions in glomerular cell density and content of synaptopodin and Wilms' tumour protein-1. It coincided with the development of mesangial expansion and glomerular sclerosis, and with the upregulation/activation both of tumour protein p53, which increased progressively throughout the study, and of p21 (also known as cyclin-dependent kinase inhibitor 1A, CIP1 and WAF1), which peaked at 4 months and decreased thereafter. CONCLUSIONS/

interpretationGlomerular cell (podocyte) apoptosis is not an early feature in the course of experimental diabetic glomerulopathy, since it is preceded by glomerular hypertrophy, which may decrease glomerular cell density to the point of inducing compensatory podocyte hypertrophy. This is associated with reduced podocyte protein expression (podocytopathy) and proteinuria, and ultimately results in apoptotic cell loss (podocytopenia), driving progression to mesangial expansion and glomerular sclerosis.

Indexed as

StreptozocinAlbuminuriaAnimalsApoptosisBlood GlucoseBody WeightCell CycleCreatinineDiabetes Mellitus, ExperimentalDiabetic NephropathiesGenes, p53Kidney GlomerulusMaleMicrofilament ProteinsPodocytesProteinuriaBlood GlucoseCreatinineMicrofilament ProteinsStreptozocinSynpo protein, rat

Identifiers

PMID17901943
OpenAlexW2156886772

What OpenQuestion holds

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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.