Evidence map›Paper›PMID 41372512›Full record

ArticleCommunications biology2025

miR-299a-5p is a mediator of fibrosis in diabetic kidney disease by regulating follistatin and cripto-1.

Ifeanyi K Nmecha, Bo Gao, Melissa MacDonald, Dan Zhang, Jason Choi, Jackie Trink, Urooj Bajwa, Joan C Krepinsky

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Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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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

8 authors.

Ifeanyi K NmechaDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.
Bo GaoDivision of Nephrology, Department of Medicine, Hamilton Centre for Kidney Research (HCKR), Centre for Metabolism, Obesity, and Diabetes Research (MODR), St. Joseph's Healthcare, Hamilton, ON, Canada.
Melissa MacDonaldDivision of Nephrology, Department of Medicine, Hamilton Centre for Kidney Research (HCKR), Centre for Metabolism, Obesity, and Diabetes Research (MODR), St. Joseph's Healthcare, Hamilton, ON, Canada.
Dan ZhangDivision of Nephrology, Department of Medicine, Hamilton Centre for Kidney Research (HCKR), Centre for Metabolism, Obesity, and Diabetes Research (MODR), St. Joseph's Healthcare, Hamilton, ON, Canada.
Jason ChoiDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.
Jackie TrinkDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.
Urooj BajwaDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada.
Joan C KrepinskyDepartment of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, ON, Canada. krepinj@mcmaster.ca.ORCID http://orcid.org/0000-0002-6761-909X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glomerular extracellular matrix protein accumulation, mediated largely by mesangial cells(MC), is a defining feature of diabetic kidney disease(DKD). Previously we showed that TGFβ1, a profibrotic cytokine in kidney fibrosis, inhibits expression of the antifibrotic follistatin through induction of microRNA-299a-5p. Whether this microRNA contributes to DKD is unknown. We show that microRNA-299a-5p is increased in mouse and human diabetic kidneys, and by high glucose in primary MC. Overexpression of microRNA-299a-5p in MC increased basal ECM protein production. Conversely, microRNA-299a-5p inhibition prevented the glucose-induced profibrotic response. Bioinformatics screening revealed that cripto-1 is also a target of microRNA-299a-5p. Induction of microRNA-299a-5p by high glucose mediated the MC fibrotic response by inhibiting follistatin and cripto-1 which led to increased activin A and TGFβ1 signaling. In vivo, microRNA-299a-5p inhibition reduced clinical markers of DKD, and was associated with increased expression of follistatin and cripto-1. Thus, microRNA-299a-5p is an important mediator of glucose-induced profibrotic responses in diabetic kidneys.

Indexed as

Diabetic NephropathiesEGF Family of ProteinsFollistatinGPI-Linked ProteinsIntercellular Signaling Peptides and ProteinsMicroRNAsNeoplasm ProteinsAnimalsEpidermal Growth FactorFibrosisGene Expression RegulationHumansMaleMembrane GlycoproteinsMesangial CellsMiceEGF Family of ProteinsEpidermal Growth FactorFollistatinGPI-Linked ProteinsIntercellular Signaling Peptides and ProteinsMembrane GlycoproteinsMicroRNAsNeoplasm ProteinsTDGF1 protein, humanTdgf1 protein, mouseTransforming Growth Factor beta1

Identifiers

PMID41372512
PMCPMC12770380

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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.