Evidence map›Paper›PMID 31593640›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2019

Exogenous miR-26a suppresses muscle wasting and renal fibrosis in obstructive kidney disease.

Aiqing Zhang, Haidong Wang, Bin Wang, Yanggang Yuan, Janet D Klein, Xiaonan H Wang

Open access · bronzeAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 76 citations in OpenAlex.

  1. Pooled it
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  12. Widespread tissue delivery of antagomiRs via intramuscular administration.Molecular therapy. Methods & clinical development · 2025
    Article
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  20. Epigenetics of Skeletal Muscle Atrophy.International journal of molecular sciences · 2024
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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

6 authors at 2 institutions in 2 countries.

Aiqing ZhangDepartment of Pediatric Nephrology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.
Haidong WangRenal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.
Bin WangRenal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.
Yanggang YuanDepartment of Nephrology, First Affiliated Hospital of Nanjing Medical University, Jiangsu Province Hospital, Nanjing, China.
Janet D KleinRenal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.
Xiaonan H WangRenal Division, Department of Medicine, Emory University, Atlanta, Georgia, USA.
Emory University · USJiangsu Province Hospital · CN

Funding

Yerkes National Primate Research Center Role of type-I IFN in regulating COVID-19 induced inflammation and pathogenesisP51OD011132 · OD · EMORY UNIVERSITY · PI Joon Sup Lee · 2012 to 2026
$167.0M
Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
MicroRNA and Muscle Wasting in UremiaR01AR060268 · NIAMS · EMORY UNIVERSITY · PI WANG, XIAONAN H · 2012 to 2016
$1.7M
NCATS NIH HHS UL1 TR000454NIAMS NIH HHS R01 AR060268NIH HHS P51 OD011132
6 · The paper itself

Abstract

Kidney fibrosis occurs in almost every type of chronic kidney disease. We found that microRNA (miR)-26a was decreased in the kidney, muscle, and exosomes of unilateral ureteral obstruction (UUO) mice. We hypothesized that exogenous miR-26 could suppresses renal fibrosis and muscle wasting in obstructive kidney disease. For this purpose, we generated exosomes that encapsulated miR-26, then injected these into skeletal muscle of UUO mice. The expression of miR-26a was elevated in serum exosomes from UUO mice following exosome-miR-26a injection. In these mice, muscle wasting has been ameliorated as evidenced by increased muscle weights. In addition, a muscle atrophy marker, myostatin, is increased in UUO muscle; provision of miR-26a abolished this increase. We detected a remote effect of exosomes containing miR-26a in UUO-induced renal fibrosis. The intervention of miR-26a attenuated UUO-induced renal fibrosis as determined by immunohistological assessment of α-smooth muscle actin and Masson's trichrome staining. Furthermore, exogenous miR-26a decreased the protein levels of 2 profibrosis proteins, connective tissue growth factor (CTGF) and TGF-β1, in UUO kidney. Our data showed that exosomes containing miR-26a prevented muscle atrophy by inhibiting the transcription factor forkhead box O1. Likewise, the exosome-carried miR-26a limited renal fibrosis by directly suppressing CTGF. Our findings provide an experimental basis for exosome-mediated therapy of muscle atrophy and renal fibrosis.-Zhang, A., Wang, H., Wang, B., Yuan, Y., Klein, J. D., Wang, X. H. Exogenous miR-26a suppresses muscle wasting and renal fibrosis in obstructive kidney disease.

Indexed as

Gene Expression RegulationAnimalsConnective Tissue Growth FactorExosomesFibrosisForkhead Box Protein O1Kidney DiseasesMaleMiceMice, Inbred C57BLMicroRNAsMuscular AtrophyUreteral ObstructionCCN2 protein, mouseConnective Tissue Growth FactorForkhead Box Protein O1Foxo1 protein, mouseMicroRNAsMirn26 microRNA, mouseCTGFexosomemuscle atrophyTGF-β1UUO

Identifiers

PMID31593640
PMCPMC6894078
OpenAlexW2979434884

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.