Evidence map›Paper›PMID 30148844›Full record

ArticlePloS one2018

Human extracellular microvesicles from renal tubules reverse kidney ischemia-reperfusion injury in rats.

James M Dominguez, Jesus H Dominguez, Danhui Xie, K J Kelly

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

James M DominguezDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Jesus H DominguezDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States of America.ORCID 0000-0002-1636-4904
Danhui XieDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States of America.
K J KellyDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, United States of America.
Richard L. Roudebush VA Medical Center · USIndiana University School of Medicine

Funding

The Postischemia Inflammatory Syndrome in the Aged KidneyR01DK082739 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI KELLY, KATHERINE J · 2010 to 2014
$1.4M
NIDDK NIH HHS R01 DK082739
6 · The paper itself

Abstract

Hypoxic acute kidney injury, a major unresolved problem, initiates, or aggravates, renal functional and structural decline. There is no treatment for hypoxic acute renal injury and its sequelae. We tested the hypothesis that human kidney tubular cells, or their extracellular vesicles (exosomes), prevent renal injury when infused intravenously 24 hours after 50 minutes of bilateral renal ischemia in Nude rats. Cells and their exosomes were from harvested human kidneys declined for transplantation. Injections of either cells or exosomes, given after 24 and 48 hours of reperfusion, preserved renal function and structure in both treatment groups. However, exosomes were superior to cells; and maintained renal vascular and epithelial networks, prevented renal oxidant stress, and apoptosis; and restrained activation of pro-inflammatory and pro-fibrogenic pathways. Exosomes worked in 24 hours, consistent with functional rather than regenerative activity. Comprehensive proteomic analysis identified 6152 renal proteins from all cellular compartments; and 628 were altered by ischemia at all cell levels, while 377 were significantly improved by exosome infusions. We conclude that renal damage from severe ischemia was broad, and human renal exosomes prevented most protein alterations. Thus, exosomes seem to acutely correct a critical and consequential abnormality during reperfusion. In their absence, renal structure and cells transition to a chronic state of fibrosis and extensive renal cell loss.

Indexed as

Acute Kidney InjuryAnimalsApoptosisCell-Derived MicroparticlesExosomesExtracellular VesiclesHumansKidney TubulesMaleRatsReperfusion Injury

Identifiers

PMID30148844
PMCPMC6110463
OpenAlexW2889264356

What OpenQuestion holds

Textmetadata
LicenceCC0
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.