Evidence map›Paper›PMID 21957176›Full record

ArticleAmerican journal of physiology. Renal physiology2012

Mast cells are required for the development of renal fibrosis in the rodent unilateral ureteral obstruction model.

Arul Veerappan, Alicia C Reid, Nathan O'Connor, Rosalia Mora, Jacqueline A Brazin, Racha Estephan, Takashi Kameue, Jie Chen, Diane Felsen, Surya V Seshan and 3 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Delayed Rectifier KBioMed research international · 2019
    Article
  6. An Adaptogen: Withaferin A AmelioratesFrontiers in pharmacology · 2018
    Article
  7. Article
  8. Article
  9. Observational
  10. E-NTPDase1/CD39 modulates renin release from heart mast cells during ischemia/reperfusion: a novel cardioprotective role.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
  11. Review
  12. Inflammatory processes in renal fibrosis.Nature reviews. Nephrology · 2014
    Review
  13. Article
  14. Review
  15. Renal interstitial fibrosis: mechanisms and evaluation.Current opinion in nephrology and hypertension · 2012
    Review
  16. Review
  17. 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

13 authors at 1 institution in 1 country.

Arul VeerappanDept. of Physiology and Biophysics, Weill Cornell Medical College, 1300 York Ave., Box 75, New York, NY 10065, USA.
Alicia C Reid
Nathan O'Connor
Rosalia Mora
Jacqueline A Brazin
Racha Estephan
Takashi Kameue
Jie Chen
Diane Felsen
Surya V Seshan
Dix P Poppas
Thomas Maack
Randi B Silver
Cornell University · US

Funding

Mast-Cell Renin and Local ANG II FormationR01DK060726 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI SILVER, RANDI BETH · 2002 to 2010
$2.9M
NIDDK NIH HHS DK060726NIDDK NIH HHS R01 DK060726
6 · The paper itself

Abstract

Mast cells are associated with inflammation and fibrosis. Whether they protect against or contribute to renal fibrosis is unclear. Based on our previous findings that mast cells can express and secrete active renin, and that angiotensin (ANG II) is profibrotic, we hypothesized that mast cells play a critical role in tubulointerstitial fibrosis. We tested this hypothesis in the 14-day unilateral ureteral obstruction (UUO) model in rats and mast cell-deficient (MCD) mice (WBB6F1-W/Wv) and their congenic controls (CC). In the 14-day UUO rat kidney, mast cell number is increased and they express active renin. Stabilizing mast cells in vivo with administration of cromolyn sodium attenuated the development of tubulointerstitial fibrosis, which was confirmed by measuring newly synthesized pepsin-soluble collagen and blind scoring of fixed trichrome-stained kidney sections accompanied by spectral analysis. Fibrosis was absent in UUO kidneys from MCD mice unlike that observed in the CC mice. Losartan treatment reduced the fibrosis in the CC UUO kidneys. The effects of mast cell degranulation and renin release were tested in the isolated, perfused kidney preparation. Mast cell degranulation led to renin-dependent protracted flow recovery. This demonstrates that mast cell renin is active in situ and the ensuing ANG II can modulate intrarenal vascular resistance in the UUO kidney. Collectively, the data demonstrate that mast cells are critical to the development of renal fibrosis in the 14-day UUO kidney. Since renin is present in human kidney mast cells, our work identifies potential targets in the treatment of renal fibrosis.

Indexed as

Angiotensin IIAnimalsCell DegranulationFibrosisHumansIn Vitro TechniquesKidneyKidney DiseasesLosartanMaleMast CellsMiceRatsReninRenin-Angiotensin SystemUreteral ObstructionAngiotensin IILosartanRenin

Identifiers

PMID21957176
PMCPMC3251335
OpenAlexW2054090757

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.