Evidence map›Paper›PMID 26661648›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Blockade of CCR2 reduces macrophage influx and development of chronic renal damage in murine renovascular hypertension.

Sonu Kashyap, Gina M Warner, Stella P Hartono, Rajendra Boyilla, Bruce E Knudsen, Adeel S Zubair, Karen Lien, Karl A Nath, Stephen C Textor, Lilach O Lerman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 43 citations in OpenAlex.

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  18. Inflammation in Hypertension.The Canadian journal of cardiology · 2020
    Review
  19. CCL2 mediates early renal leukocyte infiltration during salt-sensitive hypertension.American journal of physiology. Renal physiology · 2020
    Article
  20. Review
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

11 authors at 2 institutions in 1 country.

Sonu KashyapDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;
Gina M WarnerDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;
Stella P HartonoDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota; Mayo Medical School, Mayo Clinic, Rochester, Minnesota; and.
Rajendra BoyillaDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;
Bruce E KnudsenDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;
Adeel S ZubairMayo Medical School, Mayo Clinic, Rochester, Minnesota; and.
Karen LienDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota;
Karl A NathDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Stephen C TextorDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Lilach O LermanDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Joseph P GrandeDepartment of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota; Division of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota grande.joseph@mayo.edu.
Mayo Clinic · USWinnMed · US

Funding

MAYO CLINIC CENTER FOR TRANSLATIONAL SCIENCE ACTIVITIESUL1RR024150 · NCRR · MAYO CLINIC ROCHESTER · PI RIZZA, ROBERT A. · 2006 to 2011
$66.4M
Tissue Oxygenation in Human Renovascular HypertensionP01HL085307 · NHLBI · MAYO CLINIC ROCHESTER · PI GRANDE, JOSEPH PETER · 2007 to 2011
$10.4M
Medical Scientist Traning Program at Mayo ClinicT32GM065841 · NIGMS · MAYO CLINIC ROCHESTER · PI KAUFMANN, SCOTT H, SCHIMMENTI, LISA A · 2003 to 2022
$5.8M
CT imaging for the assessment of kidney injury distal to renal artery stenosisR01DK073608 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2006 to 2015
$3.1M
Hypoxia and inflammatory injury in human renovascular hypertensionR01DK100081 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O, TEXTOR, STEPHEN C · 2014 to 2018
$2.8M
Role of CC chemokine signaling in hyperglycemic renal artery stenosisR01AI100911 · NIAID · MAYO CLINIC ROCHESTER · PI GRANDE, JOSEPH PETER · 2013 to 2017
$2.4M
Noninvasive assessment of renal fibrosis using magnetization transfer MRIU01DK104273 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2014 to 2018
$1.8M
Mechanistic Role of CD4+ T-Cells in Atherosclerotic Renal Artery StenosisF30DK102232 · NIDDK · MAYO CLINIC ROCHESTER · PI HARTONO, STELLA P · 2014 to 2016
$133k
NCRR NIH HHS UL1 RR024150NHLBI NIH HHS P01 HL85307NIAID NIH HHS R01 AI100911NIAID NIH HHS R01 AI100911-01NIDDK NIH HHS DK104273NIDDK NIH HHS DK73608NIDDK NIH HHS F30 DK102232NIDDK NIH HHS F30 DK102232-01NIDDK NIH HHS R01 DK073608NIDDK NIH HHS R01 DK100081NIDDK NIH HHS U01 DK104273NIGMS NIH HHS T32 GM065841NIGMS NIH HHS T32 GM6584
6 · The paper itself

Abstract

Renovascular hypertension (RVH) is a common cause of both cardiovascular and renal morbidity and mortality. In renal artery stenosis (RAS), atrophy in the stenotic kidney is associated with an influx of macrophages and other mononuclear cells. We tested the hypothesis that chemokine receptor 2 (CCR2) inhibition would reduce chronic renal injury by reducing macrophage influx in the stenotic kidney of mice with RAS. We employed a well-established murine model of RVH to define the relationship between macrophage infiltration and development of renal atrophy in the stenotic kidney. To determine the role of chemokine ligand 2 (CCL2)/CCR2 signaling in the development of renal atrophy, mice were treated with the CCR2 inhibitor RS-102895 at the time of RAS surgery and followed for 4 wk. Renal tubular epithelial cells expressed CCL2 by 3 days following surgery, a time at which no significant light microscopic alterations, including interstitial inflammation, were identified. Macrophage influx increased with time following surgery. At 4 wk, the development of severe renal atrophy was accompanied by an influx of inducible nitric oxide synthase (iNOS)+ and CD206+ macrophages that coexpressed F4/80, with a modest increase in macrophages coexpressing arginase 1 and F4/80. The CCR2 inhibitor RS-102895 attenuated renal atrophy and significantly reduced the number of dual-stained F4/80+ iNOS+ and F4/80+ CD206+ but not F4/80+ arginase 1+ macrophages. CCR2 inhibition reduces iNOS+ and CD206+ macrophage accumulation that coexpress F4/80 and renal atrophy in experimental renal artery stenosis. CCR2 blockade may provide a novel therapeutic approach to humans with RVH.

Indexed as

AnimalsAntigens, DifferentiationArginaseAtrophyBenzoxazinesChemokine CCL2CytoprotectionDisease Models, AnimalHypertension, RenovascularKidneyLectins, C-TypeMacrophagesMaleMannose-Binding LectinsMannose ReceptorMice, Inbred C57BLAntigens, DifferentiationArg1 protein, mouseArginaseBenzoxazinesCcl2 protein, mouseCcr2 protein, mouseChemokine CCL2Lectins, C-TypeMannose-Binding LectinsMannose Receptormonocyte-macrophage differentiation antigenNitric Oxide Synthase Type IINos2 protein, mousePiperidinesProtective AgentsReceptors, CCR2Receptors, Cell SurfaceRS 102895CCL2CCR2hypertensionmacrophagesparenchymal cellsrenal artery stenosis

Identifiers

PMID26661648
PMCPMC4773828
OpenAlexW2272222114

What OpenQuestion holds

Textmetadata
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.