Evidence map›Paper›PMID 22048723›Full record

ReviewCurrent opinion in nephrology and hypertension2012

The kallikrein-kinin system and oxidative stress.

Yukako Kayashima, Oliver Smithies, Masao Kakoki

Abstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

33 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Kinin receptors in adipose tissue: drivers of inflammation and metabolic dysfunction in obesity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Review
  4. Review
  5. Keratin 1 modulates intestinal barrier and immune responseWorld journal of gastroenterology · 2025
    Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Kinins and Kinin Receptors in Cardiovascular and Renal Diseases.Pharmaceuticals (Basel, Switzerland) · 2021
    Review
  14. Review
  15. Acute kidney injury caused by venomous animals: inflammatory mechanisms.The journal of venomous animals and toxins including tropical diseases · 2021
    Article
  16. COVID-19 Usurps Host Regulatory Networks.Frontiers in pharmacology · 2020
    Review
  17. Review
  18. Article
  19. Article
  20. 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

3 authors at 1 institution in 1 country.

Yukako KayashimaDepartment of Pathology and Laboratory Medicine, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-7525, USA.
Oliver Smithies
Masao Kakoki
University of North Carolina at Chapel Hill · US

Funding

MODELS FOR STUDYING THE GENETICS OF HYPERTENSIONR01HL049277 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MAEDA, NOBUYO · 1992 to 2025
$17.5M
Bradykinin, Nitric Oxide and Mitochondrial DNA Damage in Diabetic ComplicationsU01DK076131 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITHIES, OLIVER · 2006 to 2010
$1.5M
NHLBI NIH HHS HL49277NHLBI NIH HHS R01 HL049277NIDDK NIH HHS DK76131NIDDK NIH HHS U01 DK076131
6 · The paper itself

Abstract

purpose of reviewThe kallikrein-kinin system (KKS) constitutes a complex multienzyme cascade that produces several bioactive kinin peptides and their derivatives including bradykinin. In addition to the classical notion of the KKS as a potent vasodilator and a mediator of inflammatory responses, recent studies suggest a link between the KKS and oxidative stress. A number of established mouse models with altered levels of KKS components opened the way to evaluate precise functions of the KKS. Here we review recent findings on the role of the KKS in cardiovascular diseases and chronic kidney diseases, and discuss potential benefits of KKS activation in these diseases. RECENT

findingsDeletion of both B1R and B2R in a diabetic mouse model exacerbates its renal phenotypes, suggesting that the KKS exerts protective effects on diabetic nephropathy by suppressing oxidative stress, presumably via nitric oxide and prostaglandins. SUMMARY: Accumulating evidence has highlighted the importance of the KKS as a protective system against oxidative stress and organ damage in the heart and kidney. The activation of the KKS by angiotensin I-converting enzyme inhibitors and vasopeptidase inhibitors is likely to be beneficial in senescence-associated cardiovascular diseases and chronic kidney diseases.

Indexed as

Kallikrein-Kinin SystemOxidative StressAngiotensin-Converting Enzyme InhibitorsAnimalsCardiovascular DiseasesEnzyme ActivationHumansKallikreinsKidney DiseasesKininsNitric OxidePeptidyl-Dipeptidase AProstaglandinsReceptors, BradykininAngiotensin-Converting Enzyme InhibitorsKallikreinsKininsNitric OxidePeptidyl-Dipeptidase AProstaglandinsReceptors, Bradykinin

Identifiers

PMID22048723
PMCPMC3657726
OpenAlexW2047808422

What OpenQuestion holds

Textmetadata
LicenceTDM
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.