Evidence map›Paper›PMID 25667212›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Cytosolic phospholipase A2α is critical for angiotensin II-induced hypertension and associated cardiovascular pathophysiology.

Nayaab S Khan, Chi Young Song, Brett L Jennings, Anne M Estes, Xiao R Fang, Joseph V Bonventre, Kafait U Malik

Open access · greenAbstract read
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 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Group V secreted phospholipase AThe Journal of biological chemistry · 2020
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Possible role for brain prostanoid pathways in the development of angiotensin II-salt hypertension in rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  12. Article
  13. 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

7 authors at 1 institution in 1 country.

Nayaab S KhanFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Chi Young SongFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Brett L JenningsFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Anne M EstesFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Xiao R FangFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Joseph V BonventreFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.).
Kafait U MalikFrom the Department of Pharmacology, College of Medicine, University of Tennessee Health Science Center, Memphis, TN (N.S.K., C.Y.S., B.L.J., A.M.E., X.R.F., K.U.M.); and Renal Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Boston, MA (J.V.B.). kmalik@uthsc.edu.
Brigham and Women's Hospital · US

Funding

Angiotensins, Prostaglandins and Adrenergic InteractionsR01HL019134 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI KAFAIT U MALIK · 1985 to 2026
$14.7M
KIDNEY INJURY MOLECULE-1 IN EPITHELIAL REPAIRR01DK072381 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2005 to 2025
$8.6M
Mechanisms of Ischemic Kidney Injury and RepairR37DK039773 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 1993 to 2021
$5.2M
NHLBI NIH HHS R01 HL019134NHLBI NIH HHS R01-HL-19134-39NIDDK NIH HHS DK072381NIDDK NIH HHS R01 DK072381NIDDK NIH HHS R37 DK039773NIDDK NIH HHS R37 DK39773
6 · The paper itself

Abstract

Angiotensin II activates cytosolic phospholipase A(2)α (cPLA2α) and releases arachidonic acid from tissue phospholipids, which mediate or modulate ≥1 cardiovascular effects of angiotensin II and has been implicated in hypertension. Because arachidonic acid release is the rate limiting step in eicosanoid production, cPLA2α might play a central role in the development of angiotensin II-induced hypertension. To test this hypothesis, we investigated the effect of angiotensin II infusion for 13 days by micro-osmotic pumps on systolic blood pressure and associated pathogenesis in wild type (cPLA2α(+/+)) and cPLA2α(-/-) mice. Angiotensin II-induced increase in systolic blood pressure in cPLA2α(+/+) mice was abolished in cPLA2α(-/-) mice; increased systolic blood pressure was also abolished by the arachidonic acid metabolism inhibitor, 5,8,11,14-eicosatetraynoic acid in cPLA2α(+/+) mice. Angiotensin II in cPLA2α(+/+) mice increased cardiac cPLA2 activity and urinary eicosanoid excretion, decreased cardiac output, caused cardiovascular remodeling with endothelial dysfunction, and increased vascular reactivity in cPLA2α(+/+) mice; these changes were diminished in cPLA2α(-/-) mice. Angiotensin II also increased cardiac infiltration of F4/80(+) macrophages and CD3(+) T lymphocytes, cardiovascular oxidative stress, expression of endoplasmic reticulum stress markers p58(IPK), and CHOP in cPLA2α(+/+) but not cPLA2α(-/-) mice. Angiotensin II increased cardiac activity of ERK1/2 and cSrc in cPLA2α(+/+) but not cPLA2α(-/-) mice. These data suggest that angiotensin II-induced hypertension and associated cardiovascular pathophysiological changes are mediated by cPLA2α activation, most likely through the release of arachidonic acid and generation of eicosanoids with predominant prohypertensive effects and activation of ≥1 signaling molecules, including ERK1/2 and cSrc.

Indexed as

Gene Expression RegulationOxidative StressAngiotensin IIAnimalsBlood PressureCytosolDisease Models, AnimalGroup IV Phospholipases A2HypertensionLipid MetabolismMiceMice, Inbred BALB CMyocardiumReal-Time Polymerase Chain ReactionRNAAngiotensin IIGroup IV Phospholipases A2RNAangiotensin IIcytosolic phospholipase A2α (cPLA2α)inflammationmiceoxidative stress

Identifiers

PMID25667212
PMCPMC4359078
OpenAlexW2041856892

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.