Evidence map›Paper›PMID 28490219›Full record

ArticleJournal of the renin-angiotensin-aldosterone system : JRAAS

Recruitment of macrophages from the spleen contributes to myocardial fibrosis and hypertension induced by angiotensin II.

Ning-Ping Wang, James Erskine, Wei-Wei Zhang, Rong-Hua Zheng, Li-Hui Zhang, Garret Duron, Julian Gendreau, Zhi-Qing Zhao

Open access · hybridAbstract read
In one paragraph

Article in Journal of the renin-angiotensin-aldosterone system : JRAAS. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

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  13. [Angiotensin Ⅱ inhibits AMPK/SIRT1 pathway by inducing oxidative stress in RAW264.7 macrophages].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  14. Review
  15. Article
  16. Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  17. Inflammatory responses mediate brain-heart interaction after ischemic stroke in adult mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  18. 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 3 institutions in 2 countries.

Ning-Ping Wang1 Cardiovascular Research Laboratory, Mercer University School of Medicine, USA.
James Erskine2 Department of Internal Medicine, Navicent Health, USA.
Wei-Wei Zhang3 Department of Physiology, Shanxi Medical University, China.
Rong-Hua Zheng3 Department of Physiology, Shanxi Medical University, China.
Li-Hui Zhang1 Cardiovascular Research Laboratory, Mercer University School of Medicine, USA.
Garret Duron1 Cardiovascular Research Laboratory, Mercer University School of Medicine, USA.
Julian Gendreau1 Cardiovascular Research Laboratory, Mercer University School of Medicine, USA.
Zhi-Qing Zhao1 Cardiovascular Research Laboratory, Mercer University School of Medicine, USA.
Mercer University · USShanxi Medical University · CNNavicent Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe purpose of this study was to determine whether macrophages migrated from the spleen are associated with angiotensin II-induced cardiac fibrosis and hypertension.

methodsSprague-Dawley rats were subjected to angiotensin II infusion in vehicle (500 ng/kg/min) for up to four weeks. In splenectomy, the spleen was removed before angiotensin II infusion. In the angiotensin II AT1 receptor blockade, telmisartan was administered by gastric gavage (10 mg/kg/day) during angiotensin II infusion. The heart and aorta were isolated for Western blot analysis and immunohistochemistry.

resultsAngiotensin II infusion caused a significant reduction in the number of monocytes in the spleen through the AT1 receptor-activated monocyte chemoattractant protein-1. Comparison of angiotensin II infusion, splenectomy and telmisartan comparatively reduced the recruitment of macrophages into the heart. Associated with this change, transforming growth factor β1 expression and myofibroblast proliferation were inhibited, and Smad2/3 and collagen I/III were downregulated. Furthermore, interstitial/perivascular fibrosis was attenuated. These modifications occurred in coincidence with reduced blood pressure. At week 4, invasion of macrophages and myofibroblasts in the thoracic aorta was attenuated and expression of endothelial nitric oxide synthase was upregulated, along with a reduction in aortic fibrosis.

conclusionsThese results suggest that macrophages when recruited into the heart and aorta from the spleen potentially contribute to angiotensin II-induced cardiac fibrosis and hypertension.

Indexed as

Angiotensin IIAnimalsAorta, ThoracicBlood PressureCell ProliferationChemokine CCL2CollagenFibrosisHypertensionMacrophagesMaleMonocytesMyocardiumMyofibroblastsNitric Oxide Synthase Type IIIPhosphorylationAngiotensin IIChemokine CCL2CollagenNitric Oxide Synthase Type IIIReceptor, Angiotensin, Type 1Smad ProteinsTransforming Growth Factor beta1Angiotensin II AT1 receptorcollagenhypertensionmacrophagesmyocardial fibrosissplenectomy

Identifiers

PMID28490219
PMCPMC5843916
OpenAlexW2613763179

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.