Evidence map›Paper›PMID 24477449›Full record

ArticleCardiovascular drugs and therapy2014

Cytochrome P450 1B1 contributes to increased blood pressure and cardiovascular and renal dysfunction in spontaneously hypertensive rats.

Brett L Jennings, David E Montanez, Michael E May, Anne M Estes, Xiao R Fang, Fariborz A Yaghini, Alie Kanu, Kafait U Malik

Abstract read
In one paragraph

Article in Cardiovascular drugs and therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Article
  3. The Expression of GenesBiomedicines · 2024
    Article
  4. Article
  5. Review
  6. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  7. Article
  8. Article
  9. Review
  10. Review
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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

8 authors at 1 institution in 1 country.

Brett L JenningsDepartment of Pharmacology, College of Medicine, University of Tennessee Health Science Center, 874 Union Avenue, Memphis, TN, 38163, USA.
David E Montanez
Michael E May
Anne M Estes
Xiao R Fang
Fariborz A Yaghini
Alie Kanu
Kafait U Malik
University of Tennessee Health Science Center · US

Funding

Angiotensins, Prostaglandins and Adrenergic InteractionsR01HL019134 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KAFAIT U MALIK · 1985 to 2026
$14.7M
Eicosanoids and carbon monoxide in neonatal cerebral microcirculationK01HL096410 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KANU, ALIE JOSEPH · 2009 to 2012
$444k
NHLBI NIH HHS K01 HL096410NHLBI NIH HHS K01-HL-96410-04NHLBI NIH HHS R01 HL019134NHLBI NIH HHS R01-HL-19134-38
6 · The paper itself

Abstract

purposeWe investigated the contribution of cytochrome P450 (CYP) 1B1 to hypertension and its pathogenesis by examining the effect of its selective inhibitor, 2,4,3',5'-tetramethoxystilbene (TMS), in spontaneously hypertensive rats (SHR).

methodsBlood pressure (BP) was measured bi-weekly. Starting at 8 weeks, TMS (600 μg/kg, i.p.) or its vehicle was injected daily. At 14 weeks, samples were collected for measurement.

resultsTMS reversed increased BP in SHR (207 ± 7 vs. 129 ± 2 mmHg) without altering BP in Wistar-Kyoto rats. Increased CYP1B1 activity in SHR was inhibited by TMS (RLU: aorta, 5.4 ± 0.7 vs. 3.7 ± 0.7; heart, 6.0 ± 0.8 vs. 3.4 ± 0.4; kidney, 411 ± 45 vs. 246 ± 10). Increased vascular reactivity, cardiovascular hypertrophy, endothelial and renal dysfunction, cardiac and renal fibrosis in SHR were minimized by TMS. Increased production of reactive oxygen species and NADPH oxidase activity in SHR, were diminished by TMS. In SHR, TMS reduced increased plasma levels of nitrite/nitrate (46.4 ± 5.0 vs. 28.1 ± 4.1 μM), hydrogen-peroxide (36.0 ± 3.7 vs. 14.1 ± 3.8 μM), and thiobarbituric acid reactive substances (6.9 ± 1.0 vs. 3.4 ± 1.5 μM). Increased plasma levels of pro-inflammatory cytokines and catecholamines, and cardiac activity of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, c-Src tyrosine kinase, and protein kinase B in SHR were also inhibited by TMS.

conclusionsThese data suggests that increased oxidative stress generated by CYP1B1 contributes to hypertension, increased cytokine production and sympathetic activity, and associated pathophysiological changes in SHR. CYP1B1 could be a novel target for developing drugs to treat hypertension and its pathogenesis.

Indexed as

AnimalsAryl Hydrocarbon HydroxylasesBlood PressureCardiovascular SystemCatecholaminesCytochrome P-450 CYP1B1CytokinesEndothelium, VascularFibrosisGenes, srcHydrogen PeroxideHypertensionHypertrophyKidneyKidney DiseasesMale2,4,3',5'-tetramethoxystilbeneAryl Hydrocarbon HydroxylasesCatecholaminesCyp1b1 protein, ratCytochrome P-450 CYP1B1CytokinesHydrogen PeroxideMitogen-Activated Protein KinasesNADPH OxidasesProto-Oncogene Proteins c-aktReactive Oxygen SpeciesStilbenesSuperoxidesThiobarbituric Acid Reactive Substances

Identifiers

PMID24477449
PMCPMC4335675
OpenAlexW2004609916

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.