Evidence map›Paper›PMID 34102217›Full record

ArticleKidney international2021

Kidney injury-mediated disruption of intestinal lymphatics involves dicarbonyl-modified lipoproteins.

Jianyong Zhong, Hai-Chun Yang, Valery Yermalitsky, Elaine L Shelton, Tadashi Otsuka, Carrie B Wiese, Linda S May-Zhang, Babak Banan, Naji Abumrad, Jiansheng Huang and 8 more

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2021. 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
1.7field-weighted citation impact, top 13% 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, 21 citations in OpenAlex.

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  11. Angiogenesis-An Emerging Role in Organ Fibrosis.International journal of molecular sciences · 2023
    Review
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  15. Review
  16. Lymphangiogenesis and Lymphatic Barrier Dysfunction in Renal Fibrosis.International journal of molecular sciences · 2022
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors at 2 institutions in 1 country.

Jianyong ZhongDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Hai-Chun YangDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Electronic address: haichun.yang@vumc.org.
Valery YermalitskyDepartment of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.
Elaine L SheltonDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Tadashi OtsukaDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Carrie B WieseDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Linda S May-ZhangDepartment of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.
Babak BananDepartment of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Naji AbumradDepartment of Surgery, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Jiansheng HuangDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Ashley B CavnarDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Annet KiraboDepartment of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.
Patricia G YanceyDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Agnes B FogoDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, Tennessee, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Kasey C VickersDepartment of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
MacRae F LintonDepartment of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Sean S DaviesDepartment of Clinical Pharmacology, Vanderbilt University, Nashville, Tennessee, USA.
Valentina KonDepartment of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA. Electronic address: valentina.kon@vumc.org.
Vanderbilt University Medical Center · USVanderbilt University · US

Funding

Non-coding RNA & Bioinformatics CoreP01HL116263 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KON, VALENTINA · 2014 to 2025
$24.7M
RESOLUTION OF GLOMERULOSCLEROSISR01DK056942 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI FOGO, AGNES B. · 2001 to 2021
$4.9M
NHLBI NIH HHS P01 HL116263NIDDK NIH HHS R01 DK056942
6 · The paper itself

Abstract

Kidney disease affects intestinal structure and function. Although intestinal lymphatics are central in absorption and remodeling of dietary and synthesized lipids/lipoproteins, little is known about how kidney injury impacts the intestinal lymphatic network, or lipoproteins transported therein. To study this, we used puromycin aminoglycoside-treated rats and NEP25 transgenic mice to show that proteinuric injury expanded the intestinal lymphatic network, activated lymphatic endothelial cells and increased mesenteric lymph flow. The lymph was found to contain increased levels of cytokines, immune cells, and isolevuglandin (a highly reactive dicarbonyl) and to have a greater output of apolipoprotein AI. Plasma levels of cytokines and isolevuglandin were not changed. However, isolevuglandin was also increased in the ileum of proteinuric animals, and intestinal epithelial cells exposed to myeloperoxidase produced more isolevuglandin. Apolipoprotein AI modified by isolevuglandin directly increased lymphatic vessel contractions, activated lymphatic endothelial cells, and enhanced the secretion of the lymphangiogenic promoter vascular endothelial growth factor-C by macrophages. Inhibition of isolevuglandin synthesis by a carbonyl scavenger reduced intestinal isolevuglandin adduct level and lymphangiogenesis. Thus, our data reveal a novel mediator, isolevuglandin modified apolipoprotein AI, and uncover intestinal lymphatic network structure and activity as a new pathway in the crosstalk between kidney and intestine that may contribute to the adverse impact of kidney disease on other organs.

Indexed as

Lymphatic VesselsVascular Endothelial Growth Factor CAnimalsApolipoprotein A-IEndothelial CellsKidneyLymphangiogenesisMiceRatsApolipoprotein A-IVascular Endothelial Growth Factor CHDLintestineisolevuglandinkidneylymphaticsreactive dicarbonyls

Identifiers

PMID34102217
PMCPMC8447488
OpenAlexW3167160392

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.