Evidence map›Paper›PMID 26573711›Full record

ArticleHypertension (Dallas, Tex. : 1979)2016

Cytochrome P450 1B1 Contributes to the Development of Atherosclerosis and Hypertension in Apolipoprotein E-Deficient Mice.

Chi Young Song, Khuzema Ghafoor, Hafiz U Ghafoor, Nayaab S Khan, Shyamala Thirunavukkarasu, Brett L Jennings, Anne M Estes, Sahar Zaidi, Dave Bridges, Patrick Tso and 2 more

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-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

20 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. International journal of hypertension · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. CYP1B1 as a therapeutic target in cardio-oncology.Clinical science (London, England : 1979) · 2020
    Article
  12. Article
  13. The Multifarious Link between Cytochrome P450s and Cancer.Oxidative medicine and cellular longevity · 2020
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Cytochrome P450: Polymorphisms and Roles in Cancer, Diabetes and AtherosclerosisAsian Pacific journal of cancer prevention : APJCP · 2018
    Review
  19. Review
  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

12 authors at 1 institution in 1 country.

Chi Young SongFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Khuzema GhafoorFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Hafiz U GhafoorFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Nayaab S KhanFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Shyamala ThirunavukkarasuFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Brett L JenningsFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Anne M EstesFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Sahar ZaidiFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Dave BridgesFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Patrick TsoFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Frank J GonzalezFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.).
Kafait U MalikFrom the Department of Pharmacology (C.Y.S., K.G., H.U.G., N.S.K., S.T., B.L.J., A.M.E., S.Z., K.U.M.) and Department of Physiology and Pediatrics (D.B.), College of Medicine, University of Tennessee Health Science Center, Memphis; Department of Pathobiology and Molecular Medicine, University of Cincinnati, OH (P.T.); and Center for Cancer Research, Laboratory of Metabolism, National Cancer Institute, Bethesda, MD (F.J.G.). kmalik@uthsc.edu.
University of Cincinnati · US

Funding

Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
Xenobiotic ReceptorsZIABC005708 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK J · 2009 to 2025
$16.4M
LIPID, LIPOPROTEIN, AND GLUCOSE METABOLISM COREU24DK059630 · NIDDK · UNIVERSITY OF CINCINNATI · PI TSO, PATRICK · 2001 to 2015
$12.9M
Lipid profile, lipoprotein and apolipoprotein composition, and intestinal fat absorption efficiency in germ-free and conventional miceU2CDK059630 · NIDDK · UNIVERSITY OF CINCINNATI · PI LIU, MIN · 2016 to 2021
$4.9M
Eicosanoid-Induced Vascular Growth During InjuryR01HL079109 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI MALIK, KAFAIT U · 2005 to 2015
$3.3M
Regulation of Lipid Storage by mTORC1R01DK107535 · NIDDK · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI BRIDGES, DAVE · 2016 to 2020
$1.7M
TRANSCRIPTIONAL REGULATION OF GENES ENCODING XENOBIOTIC METABOLIZING ENZYMESZ01BC005561 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI GONZALEZ, FRANK · 1996 to 2008
$754k
NHLBI NIH HHS R01HL079109-08NIDDK NIH HHS DK059630NIDDK NIH HHS P30 DK020572NIDDK NIH HHS R01 DK107535
6 · The paper itself

Abstract

Cytochrome P450 (CYP) 1B1 contributes to vascular smooth muscle cell growth and hypertension in male mice. This study was conducted to determine the contribution of CYP1B1 to the development of atherosclerosis and hypertension and associated pathogenesis in 8-week-old male apolipoprotein E-deficient (ApoE(-/-)/Cyp1b1(+/+)), and ApoE- and CYP1B1-deficient (ApoE(-/-)/Cyp1b1(-/-)) mice fed a normal or atherogenic diet for 12 weeks. A separate group of ApoE(-/-)/Cyp1b1(+/+) mice on an atherogenic diet was injected every third day with the CYP1B1 inhibitor, 2,3',4,5'-tetramethoxystilbene (300 μg/kg), or its vehicle, dimethyl sulfoxide (30 μL, IP); systolic blood pressure was measured by the tail cuff method. After 12 weeks, mice were euthanized, blood collected for lipid analysis, and aortas harvested for measuring lesions and remodeling, and for infiltration of inflammatory cells by histological and immunohistochemical analysis, respectively, and for reactive oxygen species production. Blood pressure, areas of lipids and collagen deposition, elastin breaks, infiltration of macrophages and T lymphocytes, reactive oxygen species generation in the aorta, and plasma lipid levels were increased in ApoE(-/-)/Cyp1b1(+/+) mice on an atherogenic diet; these changes were minimized in mice given 2,3',4,5'-tetramethoxystilbene, and in ApoE(-/-)/Cyp1b1(-/-) mice on an atherogenic diet; absorption/production of lipids remained unaltered in these mice. These data suggest that aortic lesions, hypertension, and associated pathogenesis in ApoE(-/-)/Cyp1b1(+/+) mice on an atherogenic diet are most likely dependent on CYP1B1-generated oxidative stress and increased plasma lipid levels independent of blood pressure and absorption of lipids. CYP1B1 could serve as a novel target for developing drugs to treat atherosclerosis and hypertension caused by hypercholesterolemia.

Indexed as

Gene Expression RegulationAnimalsApolipoproteins EAtherosclerosisBlood PressureCytochrome P-450 CYP1B1Disease Models, AnimalEndothelium, VascularHypertensionMaleMiceMice, KnockoutRNAVasodilationApolipoproteins ECytochrome P-450 CYP1B1RNAapolipoprotein E, deficiencycytochrome P450 1B1diet, atherogenicplasma lipidsvascular, remodeling

Identifiers

PMID26573711
PMCPMC4672747
OpenAlexW2181165254

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.