Evidence map›Paper›PMID 25733239›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Thromboxane prostanoid receptors enhance contractions, endothelin-1, and oxidative stress in microvessels from mice with chronic kidney disease.

Cheng Wang, Zaiming Luo, Donald Kohan, Anton Wellstein, Pedro A Jose, William J Welch, Christopher S Wilcox, Dan Wang

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

Article in Hypertension (Dallas, Tex. : 1979), 2015. 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
2.3field-weighted citation impact, top 12% 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, 26 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Diverse associations between oxidative stress and thromboxane AHypertension research : official journal of the Japanese Society of Hypertension · 2019
    Article
  8. Review
  9. Article
  10. Article
  11. NRF2 prevents hypertension, increased ADMA, microvascular oxidative stress, and dysfunction in mice with two weeks of ANG II infusion.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  12. Review
  13. Downregulation of Thromboxane AAdvances in pharmacological sciences · 2017
    Article
  14. Article
  15. Article
  16. Endothelial prostaglandin DJournal of the renin-angiotensin-aldosterone system : JRAAS
    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

8 authors at 2 institutions in 2 countries.

Cheng WangFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Zaiming LuoFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Donald KohanFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Anton WellsteinFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Pedro A JoseFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
William J WelchFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Christopher S WilcoxFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.).
Dan WangFrom the Hypertension, Kidney and Vascular Research Center and Division of Nephrology and Hypertension, Department of Medicine (C.W., Z.L., W.J.W., C.S.W., D.W.) and Department of Oncology, Lombardi Cancer Center (A.W.), Georgetown University, Washington, DC; Department of Nephrology, The Third Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China (C.W.); Division of Nephrology, Department of Medicine, University of Utah, Salt Lake City (D.K.); and Division of Nephrology, Department of Medicine and Department of Physiology, University of Maryland, Baltimore, MD (P.A.J.). dw32@georgetown.edu.
Sun Yat-sen University · CNThird Affiliated Hospital of Sun Yat-sen University · CN

Funding

Renal Vascular Oxidative Stress in HypertensionP01HL068686 · NHLBI · GEORGETOWN UNIVERSITY · PI JOSE, PEDRO A., SANDBERG, KATHRYN L · 2001 to 2017
$28.8M
REGULATION OF RENAL FUNCTION AND BP BY THROMBOXANER37DK036079 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 2003 to 2012
$5.2M
NITRIC OXIDE SYNTHASE IN THE JUXTAGLOMERULAR APPARATUSR01DK049870 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 1994 to 2014
$4.6M
OXIDATIVE STRESS AND KIDNEY OXYGEN USAGER01HL089583 · NHLBI · GEORGETOWN UNIVERSITY · PI WELCH, WILLIAM J · 2008 to 2012
$1.9M
NEPHROLOGY AND HYPERTENSION TRAINING GRANTT32DK059274 · NIDDK · GEORGETOWN UNIVERSITY · PI WILCOX, CHRISTOPHER S · 2001 to 2011
$1.9M
Regulation of Renal Function and BP by ThromboxaneR01DK109272 · NIDDK · GEORGETOWN UNIVERSITY · PI WELCH, WILLIAM J, WILCOX, CHRISTOPHER S · 2016 to 2019
$1.4M
REGULATION OF RENAL FUNCTION AND BP BY THROMBOXANER01DK036079 · NIDDK · UNIVERSITY OF FLORIDA · PI WILCOX, CHRISTOPHER S · 1986 to 2002
$830k
NHLBI NIH HHS HL-089583NHLBI NIH HHS HL-68686NHLBI NIH HHS P01 HL068686NHLBI NIH HHS R01 HL089583NIDDK NIH HHS DK-036079NIDDK NIH HHS DK-049870NIDDK NIH HHS R01 DK036079NIDDK NIH HHS R01 DK049870NIDDK NIH HHS R01 DK109272NIDDK NIH HHS R37 DK036079NIDDK NIH HHS T32 DK059274
6 · The paper itself

Abstract

Cardiovascular disease is frequent in chronic kidney disease and has been related to angiotensin II, endothelin-1 (ET-1), thromboxane A2, and reactive oxygen species (ROS). Because activation of thromboxane prostanoid receptors (TP-Rs) can generate ROS, which can generate ET-1, we tested the hypothesis that chronic kidney disease induces cyclooxygenase-2 whose products activate TP-Rs to enhance ET-1 and ROS generation and contractions. Mesenteric resistance arterioles were isolated from C57/BL6 or TP-R+/+ and TP-R-/- mice 3 months after SHAM-operation (SHAM) or surgical reduced renal mass (RRM, n=6/group). Microvascular contractions were studied on a wire myograph. Cellular (ethidium: dihydroethidium) and mitochondrial (mitoSOX) ROS were measured by fluorescence microscopy. Mice with RRM had increased excretion of markers of oxidative stress, thromboxane, and microalbumin; increased plasma ET-1; and increased microvascular expression of p22(phox), cyclooxygenase-2, TP-Rs, preproendothelin and endothelin-A receptors, and increased arteriolar remodeling. They had increased contractions to U-46,619 (118 ± 3 versus 87 ± 6, P<0.05) and ET-1 (108 ± 5 versus 89 ± 4, P<0.05), which were dependent on cellular and mitochondrial ROS, cyclooxygenase-2, and TP-Rs. RRM doubled the ET-1-induced cellular and mitochondrial ROS generation (P<0.05). TP-R-/- mice with RRM lacked these abnormal structural and functional microvascular responses and lacked the increased systemic and the increased microvascular oxidative stress and circulating ET-1. In conclusion, RRM leads to microvascular remodeling and enhanced ET-1-induced cellular and mitochondrial ROS and contractions that are mediated by cyclooxygenase-2 products activating TP-Rs. Thus, TP-Rs can be upstream from enhanced ROS, ET-1, microvascular remodeling, and contractility and may thereby coordinate vascular dysfunction in chronic kidney disease.

Indexed as

Oxidative StressVasoconstrictionAnimalsArteriolesDisease Models, AnimalEndothelin-1Gene Expression RegulationKidneyMaleMiceMice, Inbred C57BLReactive Oxygen SpeciesReal-Time Polymerase Chain ReactionReceptors, ThromboxaneRenal CirculationRenal Insufficiency, ChronicEndothelin-1Reactive Oxygen SpeciesReceptors, ThromboxaneRNAcyclooxygenasemitochondriaoxidative stressthromboxanevascular remodeling

Identifiers

PMID25733239
PMCPMC4990073
OpenAlexW2107687115

What OpenQuestion holds

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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.