Evidence map›Paper›PMID 22811485›Full record

ArticleAmerican journal of physiology. Renal physiology2012

Depletion of endogenous kallistatin exacerbates renal and cardiovascular oxidative stress, inflammation, and organ remodeling.

Yuying Liu, Grant Bledsoe, Makato Hagiwara, Bo Shen, Lee Chao, Julie Chao

Abstract 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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 46 citations in OpenAlex.

  1. Kallistatin levels in HIV-infected patients and effects of statin therapy.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2017
    Trial
  2. Review
  3. Clinical Significance of Serum Kallistatin and ENOX1 Levels in Patients with Coronary Heart Disease.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2021
    Article
  4. Innate immunity in diabetic kidney disease.Nature reviews. Nephrology · 2020
    Review
  5. Article
  6. Review
  7. Article
  8. Observational
  9. Review
  10. Review
  11. Article
  12. Protective Role of Kallistatin in Vascular and Organ Injury.Hypertension (Dallas, Tex. : 1979) · 2016
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

6 authors at 2 institutions in 1 country.

Yuying LiuDepartment of Biochemistry and Molecular Biology, Medical University of South Carolina, 173 Ashley Ave, Charleston, SC 29425-2211, USA. chaoj@musc.edu
Grant Bledsoe
Makato Hagiwara
Bo Shen
Lee Chao
Julie Chao
Medical University of South Carolina · USCharleston Southern University · US

Funding

Regulation and Function of Tissue KallikreinR01HL029397 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1986 to 2012
$3.9M
RENAL KALLIKREIN-BINDING PROTEIN IN HYPERTENSIONR01HL044083 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI CHAO, JULIE · 1990 to 2008
$2.1M
MUSC FACIL EXPANSION &RENOV: SLE C06RR015455 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI RAYMOND, JOHN R · 2002 to 2002
$2.0M
NCRR NIH HHS C06-RR-015455NHLBI NIH HHS HL-29397NHLBI NIH HHS HL-44083
6 · The paper itself

Abstract

Kallistatin (KS) levels are reduced in the kidney and blood vessels under oxidative stress conditions. To determine the function of endogenous KS in the renal and cardiovascular systems, KS levels were depleted by daily injection of anti-rat KS antibody into DOCA-salt hypertensive rats for 10 days. Administration of anti-KS antibody resulted in reduced KS levels in the circulation but increased levels of serum thiobarbituric acid reactive substances (an indicator of lipid peroxidation) as well as superoxide formation in the aorta. Moreover, anti-KS antibody injection resulted in increased NADH oxidase activity and superoxide production but decreased nitric oxide levels in the kidney and heart. Endogenous KS blockade aggravated renal dysfunction, damage, hypertrophy, inflammation, and fibrosis as evidenced by decreased creatinine clearance and increased serum creatinine, blood urea nitrogen and urinary protein levels, tubular dilation, protein cast formation, glomerulosclerosis, glomerular enlargement, inflammatory cell accumulation, and collagen deposition. In addition, rats receiving anti-KS antibody had enhanced cardiac injury as indicated by cardiomyocyte hypertrophy, inflammation, myofibroblast accumulation, and fibrosis. Renal and cardiac injury caused by endogenous KS depletion was accompanied by increases in the expression of the proinflammatory genes tumor necrosis factor-α and intercellular adhesion molecule-1 and the profibrotic genes collagen I and III, transforming growth factor-β, and tissue inhibitor of metalloproteinase-1. Taken together, these results implicate an important role for endogenous KS in protection against salt-induced renal and cardiovascular injury in rats by suppressing oxidative stress, inflammation, hypertrophy, and fibrosis.

Indexed as

AnimalsDesoxycorticosteroneHypertensionInflammationKidneyKidney DiseasesLipid PeroxidationMaleMultienzyme ComplexesNADH, NADPH OxidoreductasesOxidative StressRatsRats, WistarSerpinsSodium Chloride, DietarySuperoxidesDesoxycorticosteronekallistatinMultienzyme ComplexesNADH, NADPH OxidoreductasesNADH oxidaseSerpinsSodium Chloride, DietarySuperoxides

Identifiers

PMID22811485
PMCPMC3469672
OpenAlexW2108487693

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.