Evidence map›Paper›PMID 41481368›Full record

ArticleKidney3602026

The Renal Micro-RNA Expression Profile of Pkd1RC/RC Mice Changes Longitudinally with the Progression of the Disease.

Nalin Sharma, Jamie Zheng, Yahya Alsawaf, Santu K Singha, Xiaohong Xu, Youwen Zhang, Ivan Vuckovic, Slobodan Macura, Christian Hanna, Marie C Hogan and 2 more

Abstract read
In one paragraph

Article in Kidney360, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Article
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

12 authors.

Nalin SharmaDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.
Jamie ZhengDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0009-0000-1514-2536
Yahya AlsawafDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0009-0006-1425-0002
Santu K SinghaDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.
Xiaohong XuDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0009-0007-2370-1714
Youwen ZhangDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.
Ivan VuckovicMetabolomics Core, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0001-7806-7238
Slobodan MacuraDepartment of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-6054-5163
Christian HannaDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-9956-8696
Marie C HoganDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0003-3031-8522
Alfonso EirinDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-3864-9644
Maria V IrazabalDivision of Nephrology and Hypertension, Department of Medicine, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0002-9904-7778

Funding

Role of homocysteine metabolism, endothelial function and microvascular rarefaction on renal disease severity and progression in ADPKDR01DK128017 · NIDDK · MAYO CLINIC ROCHESTER · PI IRAZABAL, MARIA V · 2021 to 2024
$2.4M
Role of mitochondrial microRNAs (mitomiRs) in endogenous renal repairR01DK129240 · NIDDK · MAYO CLINIC ROCHESTER · PI Alfonso Eirin · 2023 to 2026
$1.8M
Role of Fumarate and Nrf2 response in the pathogenesis of Autosomal Dominant Polycystic Kidney DiseaseR21DK118391 · NIDDK · MAYO CLINIC ROCHESTER · PI IRAZABAL, MARIA V · 2018 to 2020
$586k
Congressionally Directed Medical Research Programs PR221810NIDDK NIH HHS DK118391NIDDK NIH HHS DK128017NIDDK NIH HHS DK129240NIDDK NIH HHS R01 DK128017NIDDK NIH HHS R01 DK129240NIDDK NIH HHS R21 DK118391
6 · The paper itself

Abstract

key pointsExperimental autosomal dominant polycystic kidney disease is associated with longitudinal changes in the kidney micro-RNA and mRNA profiles. Alterations in cellular transport, a feature of CKD, and a common biological process within polycystic kidney disease models and human autosomal dominant polycystic kidney disease, is present from early stages. Early versus late micro-RNA expression changes in autosomal dominant polycystic kidney disease could be targeted for a more tailored therapeutic intervention in the disease.

backgroundAutosomal dominant polycystic kidney disease (ADPKD) is characterized by the progressive development and enlargement of bilateral kidney cysts, which often leads to kidney failure. This study comprehensively characterized the expression profile of micro-RNAs (miRNAs) and their target genes in Pkd1RC/RC mice and further compared them with other murine models of polycystic kidney disease (PKD) and a model of CKD and individuals with ADPKD.

methodsPkd1RC/RC and wild-type (WT) mice ( n =10 each, five males and five females) were studied at 1, 6, and 12 months. At each time point, kidney volume was determined in vivo (magnetic resonance imaging), followed by ex vivo histomorphometric analyses. In randomly selected Pkd1RC/RC and WT mouse kidneys ( n =5/genotype, at 1 and 12 months), miRNA-sequencing (seq) was performed, followed by mRNA-seq, integrated (miRNA-seq/mRNA-seq analysis), and functional analysis of miRNA target genes. Venn diagrams were constructed to identify overlapping and novel differentially expressed (DE) miRNAs in Pkd1RC/RC and other commonly used murine models of PKD, diabetic kidney disease, and individuals with ADPKD.

resultsmiRNA-seq analysis identified 41 and 181 miRNAs DE in Pkd1RC/RC versus WT kidneys at 1 and 12 months, respectively, which were confirmed by quantitative PCR. Target genes of miRNAs DE in Pkd1RC/RC at early stages encoded for proteins mainly implicated in cell proliferation and α -ketoglutarate ( α -KG) transport, whereas those DE at late stages encoded for transport proteins involved in proinflammatory and metabolic processes. Urine α -KG concentration ( 1 H nuclear magnetic resonance spectroscopy), its fractional excretion, and tissue levels were higher in Pkd1RC/RC during the entire course of the disease and associated with decreased protein expression of α -KG transporters sodium-coupled dicarboxylate transporter 3 and organic anion transporter 1. We further identified common DE miRNAs among murine models of PKD, diabetic kidney disease, and previous reports in individuals with ADPKD, as well as several novel miRNAs DE in early and late Pkd1RC/RC kidneys, which have not been previously reported in either other murine models of PKD or patients with ADPKD.

conclusionsOur study demonstrates that the renal miRNA expression profile changes longitudinally with the progression of the disease and might suggest that the post-transcriptional regulation of α -KG transport could represent a novel early feature of the disease.

Indexed as

KidneyMicroRNAsPolycystic Kidney, Autosomal DominantTRPP Cation ChannelsAnimalsDisease Models, AnimalDisease ProgressionFemaleGene Expression ProfilingMaleMiceMicroRNAsTRPP Cation ChannelsmRNApolycystic kidney disease

Identifiers

PMID41481368
PMCPMC13337173

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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 OpenQuestion graph.