Evidence map›Paper›PMID 21718676›Full record

ArticleThe American journal of pathology2011

Inhibiting angiotensin-converting enzyme promotes renal repair by limiting progenitor cell proliferation and restoring the glomerular architecture.

Ariela Benigni, Marina Morigi, Paola Rizzo, Elena Gagliardini, Cinzia Rota, Mauro Abbate, Serena Ghezzi, Andrea Remuzzi, Giuseppe Remuzzi

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02682459 (A Pilot, Prospective, Randomized, Open-label, Blinded Endpoint), which is not on this map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
5.6field-weighted citation impact, top 3% 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.

NCT02682459 phase2unknown statusnot on this mapstarted 2016, after this paper: background citation

A Pilot, Prospective, Randomized, Open-label, Blinded Endpoint (Probe) Histopathology Trial to Assess the Effects of ACE- Inhibition Therapy on Glomerular Proliferative Lesions in Patients With Extracapillary Glomerulonephritis

TypeinterventionalSponsorMonia LoriniRan2016 to 2019Enrolled22ConditionsExtracapillary GlomerulonephritisArmsLisinopril
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 106 citations in OpenAlex.

  1. Article
  2. Article
  3. Multiomics profiling of mouse polycystic kidney disease progression at a single-cell resolution.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Mechanisms of podocyte injury and implications for diabetic nephropathy.Clinical science (London, England : 1979) · 2022
    Article
  8. Molecular Mechanisms of Kidney Injury and Repair.International journal of molecular sciences · 2022
    Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Cell Cycle Dysregulation and Renal Fibrosis.Frontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Article
  16. Cells of NG2 lineage increase in glomeruli of mice following podocyte depletion.American journal of physiology. Renal physiology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. MicroRNAs as Master Regulators of Glomerular Function in Health and Disease.Journal of the American Society of Nephrology : JASN · 2017
    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

9 authors at 2 institutions in 1 country.

Ariela BenigniMario Negri Institute for Pharmacological Research, Centro Anna Maria Astori, Bergamo, Italy.
Marina Morigi
Paola Rizzo
Elena Gagliardini
Cinzia Rota
Mauro Abbate
Serena Ghezzi
Andrea Remuzzi
Giuseppe Remuzzi
Mario Negri Institute for Pharmacological Research · ITUniversity of Bergamo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that angiotensin-converting enzyme inhibitor (ACEi) renoprotection in Munich Wistar Frömter (MWF) rats, which develop progressive glomerular injury, was associated with podocyte repopulation and preservation of glomerular architecture. Here, we studied the time course of the lesions, their cellular components, and the effect of ACEi. Early glomerular lesions were synechiae, followed by extracapillary crescents and glomerulosclerosis. The majority of cells forming crescents were claudin1(+) parietal epithelial cells and, to a lesser extent, WT1(+) podocytes, both in active proliferation. In crescents, cells expressing the metanephric mesenchyme marker NCAM were also found. Three distinct populations of parietal epithelial cells were identified in the rat Bowman's capsule: NCAM(+)WT1(-) cells, also expressing progenitor cell marker CD24, and NCAM(+)WT1(+) and NCAM(-)WT1(+) cells, the latter population representing parietal podocytes. After exposure to inductive medium, cultured parietal epithelial cells that were obtained by capsulated glomeruli generated podocytes, documenting their progenitor nature. Mitotic activity of cultured renal progenitors was induced by angiotensin II through the down-regulation of cell cycle inhibitor C/EBPδ expression. Treatment with ACEi reduced number and extension of crescents and glomerulosclerosis in MWF rats. Renoprotection was accomplished through the limitation of NCAM(+) progenitor proliferation via the modulation of C/EBPδ. Thus, chaotic migration and proliferation of the Bowman's capsule progenitor cells pave the way to crescent formation and subsequent sclerosis. ACEi, by moderating progenitor cell activation, restores glomerular architecture and prevents renal disease progression.

Indexed as

Angiotensin-Converting Enzyme InhibitorsAnimalsCell ProliferationCreatinineHumansKidneyKidney Failure, ChronicKidney GlomerulusMaleMicroscopy, ImmunoelectronMitosisPodocytesRatsRats, WistarStem CellsTime FactorsAngiotensin-Converting Enzyme InhibitorsCreatinine

Identifiers

PMID21718676
PMCPMC3157222
OpenAlexW2114370669

What OpenQuestion holds

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Registered trials

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.