Evidence map›Paper›PMID 19190676›Full record

ReviewKidney international2009

The kallikrein-kinin system in health and in diseases of the kidney.

Masao Kakoki, Oliver Smithies

Open access · bronzeAbstract readReview
In one paragraph

Review in Kidney international, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 105 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. A modular map of Bradykinin-mediated inflammatory signaling network.Journal of cell communication and signaling · 2022
    Article
  12. Favorable therapeutic efficacy of low-density lipoprotein apheresis for nephrotic syndrome with impaired renal function.Therapeutic apheresis and dialysis : official peer-reviewed journal of the International Society for Apheresis, the Japanese Society for Apheresis, the Japanese Society for Dialysis Therapy · 2022
    Observational
  13. Review
  14. A Robust Bioassay of the Human Bradykinin BPharmaceuticals (Basel, Switzerland) · 2021
    Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  20. COVID-19 Usurps Host Regulatory Networks.Frontiers in pharmacology · 2020
    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

2 authors at 1 institution in 1 country.

Masao KakokiDepartment of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC 27599-7525, USA. mkakoki@med.unc.edu
Oliver Smithies
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
Duke-UNC-Stanford AMDC UnitU01HL070523 · NHLBI · DUKE UNIVERSITY · PI COFFMAN, THOMAS M · 2001 to 2005
$3.7M
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
Genetic Control of Protein Structure and SynthesisR01HL071266 · NHLBI · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI SMITHIES, OLIVER · 2002 to 2005
$1.5M
NHLBI NIH HHS HL49277NHLBI NIH HHS HL70523NHLBI NIH HHS HL71266NHLBI NIH HHS R01 HL049277NHLBI NIH HHS R01 HL071266NHLBI NIH HHS U01 HL070523NIDDK NIH HHS U01 DK076131
6 · The paper itself

Abstract

Since kallikrein was discovered as a vasodilatory substance in human urine, the kallikrein-kinin system (KKS) has been considered to play a physiological role in controlling blood pressure. Gene targeting experiments in mice in which the KKS has been inactivated to varying degrees have, however, questioned this role, because basal blood pressures are not altered. Rather, these experiments have shown that the KKS has a different and important role in preventing changes associated with normal senescence in mice, and in reducing the nephropathy and accelerated senescence-associated phenotypes induced in mice by diabetes. Other experiments have shown that the KKS suppresses mitochondrial respiration, partly by nitric oxide and prostaglandins, and that this suppression may be a key to understanding how the KKS influences senescence-related diseases. Here we review the logical progression and experimental data leading to these conclusions, and discuss their relevance to human conditions.

Indexed as

AgingCell RespirationDiabetic NephropathiesHumansKallikrein-Kinin SystemKidney Diseases

Identifiers

PMID19190676
PMCPMC3733452
OpenAlexW2004903527

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.