Evidence map›Paper›PMID 21832206›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2011

Renal oxidative stress, oxygenation, and hypertension.

Fredrik Palm, Lina Nordquist

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 91 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025
    Review
  10. Article
  11. Review
  12. Review
  13. Article
  14. Bioactive Peptides fromMolecules (Basel, Switzerland) · 2023
    Article
  15. Article
  16. Review
  17. Review
  18. Cysteine as a Multifaceted Player in Kidney, theMolecules (Basel, Switzerland) · 2022
    Review
  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

2 authors at 1 institution in 1 country.

Fredrik PalmDept. of Medical Cell Biology, Uppsala Univ., Biomedical Center, Box 571, 751 23 Uppsala, Sweden. Fredrik.Palm@mcb.uu.se
Lina Nordquist
Uppsala University · SE

Funding

NITRIC OXIDE AND OXYGENATION IN DIABETIC KIDNEYSK99DK077858 · NIDDK · GEORGETOWN UNIVERSITY · PI PALM, NILS AXEL FREDRIK · 2007 to 2007
$90k
NIDDK NIH HHS K99/R00/DK077858
6 · The paper itself

Abstract

Hypertension is closely associated with progressive kidney dysfunction, manifested as glomerulosclerosis, interstitial fibrosis, proteinuria, and eventually declining glomerular filtration. The postulated mechanism for development of glomerulosclerosis is barotrauma caused by increased capillary pressure, but the reason for development of interstitial fibrosis and the subsequently reduced kidney function is less clear. However, it has been hypothesized that tissue hypoxia induces fibrogenesis and progressive renal failure. This is very interesting, since recent reports highlight several different mechanisms resulting in altered oxygen handling and availability in the hypertensive kidney. Such mechanisms include decreased renal blood flow due to increased vascular tone induced by ANG II that limits oxygen delivery and increases oxidative stress, resulting in increased mitochondrial oxygen usage, increased oxygen usage for tubular electrolyte transport, and shunting of oxygen from arterial to venous blood in preglomerular vessels. It has been shown in several studies that interventions to prevent oxidative stress and to restore kidney tissue oxygenation prevent progression of kidney dysfunction. Furthermore, inhibition of ANG II activity, by either blocking ANG II type 1 receptors or angiotensin-converting enzyme, or by preventing oxidative stress by administration of antioxidants also results in improved blood pressure control. Therefore, it seems likely that tissue hypoxia in the hypertensive kidney contributes to progression of kidney damage, and perhaps also persistence the high blood pressure.

Indexed as

Oxidative StressOxygen ConsumptionAngiotensin IIAnimalsAntioxidantsDisease ProgressionFibrosisHumansHypertensionHypoxiaKidneyKidney DiseasesOxygenReactive Oxygen SpeciesAngiotensin IIAntioxidantsOxygenReactive Oxygen Species

Identifiers

PMID21832206
PMCPMC3213938
OpenAlexW2065525967

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.