Evidence map›Paper›PMID 29997302›Full record

ArticleJCI insight2018

Repetitive ischemic injuries to the kidneys result in lymph node fibrosis and impaired healing.

Omar H Maarouf, Mayuko Uehara, Vivek Kasinath, Zhabiz Solhjou, Naima Banouni, Baharak Bahmani, Liwei Jiang, Osman A Yilmam, Indira Guleria, Scott B Lovitch and 6 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.5field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  17. UAB-UCSD O'Brien Center for Acute Kidney Injury Research.American journal of physiology. Renal physiology · 2021
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Omar H MaaroufTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Mayuko UeharaTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Vivek KasinathTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Zhabiz SolhjouTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Naima BanouniTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Baharak BahmaniTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Liwei JiangTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Osman A YilmamTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Indira GuleriaTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Scott B LovitchDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jane L GroganDepartment of Cancer Immunology, Genentech, Inc., South San Francisco, California, USA.
Paolo FiorinaNephrology Division, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Peter T SageTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jonathan S BrombergDepartment of Surgery, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Martina M McGrathTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Reza AbdiTransplantation Research Center, Renal Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Brigham and Women's Hospital · USBoston Children's Hospital · USUniversity of Maryland, Baltimore · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
Induction and Migration of Regulatory T Cells: Role of LymphotoxinR01AI062765 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BROMBERG, JONATHAN S · 2005 to 2019
$5.6M
Lymph Node Structure and Function in Tolerance: Role of LamininsR01AI114496 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI BROMBERG, JONATHAN S · 2015 to 2024
$4.2M
Organ Design and Engineering Training Program (ODET Program)T32EB016652 · NIBIB · BRIGHAM AND WOMEN'S HOSPITAL · PI BONVENTRE, JOSEPH VINCENT · 2014 to 2023
$3.5M
Regulatory T Cells and Lymphatic Endothelial Cells: Regulatory Interactions for Migration and SuppressionR37AI062765 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI Jonathan S Bromberg · 2021 to 2026
$2.9M
Protection of organ transplant from ischemia reperfusion injuriesR01AI126596 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI ABDI, REZA · 2016 to 2020
$2.6M
NIAID NIH HHS R01 AI114496NIAID NIH HHS R01 AI126596NIAID NIH HHS R37 AI062765NIBIB NIH HHS T32 EB016652NIDDK NIH HHS P30 DK079337
6 · The paper itself

Abstract

The contribution of the kidney-draining lymph node (KLN) to the pathogenesis of ischemia-reperfusion injury (IRI) of the kidney and its subsequent recovery has not been explored in depth. In addition, the mechanism by which repetitive IRI contributes to renal fibrosis remains poorly understood. Herein, we have found that IRI of the kidney is associated with expansion of high endothelial venules (HEVs) and activation of fibroblastic reticular cells (FRCs) in the KLN, as demonstrated by significant expansion in the extracellular matrix. The lymphotoxin α signaling pathway mediates activation of FRCs, and chronic treatment with lymphotoxin β receptor-immunoglobulin fusion protein (LTβr-Ig) resulted in marked alteration of the KLN as well as augmentation of renal fibrosis. Depletion of FRCs reduced T cell activation in the KLN and ameliorated renal injury in acute IRI. Repetitive renal IRI was associated with senescence of FRCs, fibrosis of the KLN, and renal scarring, which were ameliorated by FRC administration. Therefore, our study emphasizes the critical role of FRCs in both the initiation and repair phases of injury following IRI of the kidney.

Indexed as

Acute Kidney InjuryAnimalsDisease Models, AnimalFibrosisHomeodomain ProteinsImmunoglobulinsKidneyLymph NodesLymphotoxin beta ReceptorMaleMiceMice, Inbred C57BLMice, KnockoutReperfusion InjurySignal TransductionHomeodomain ProteinsImmunoglobulinsLymphotoxin beta ReceptorRAG-1 proteinChronic kidney diseaseFibrosisNephrology

Identifiers

PMID29997302
PMCPMC6124521
OpenAlexW2837437831

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.