Evidence map›Paper›PMID 31614781›Full record

ArticleInternational journal of molecular sciences2019

Renal Artery Stenosis Alters Gene Expression in Swine Scattered Tubular-Like Cells.

Arash Aghajani Nargesi, Xiang-Yang Zhu, Yuanhang Liu, Hui Tang, Kyra L Jordan, Lilach O Lerman, Alfonso Eirin

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 23 citations in OpenAlex.

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  6. Role of mitochondria in endogenous renal repair.Clinical science (London, England : 1979) · 2024
    Review
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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

7 authors at 1 institution in 1 country.

Arash Aghajani NargesiDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. arash.aan@gmail.com.
Xiang-Yang ZhuDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. zhu.xiangyang@mayo.edu.
Yuanhang LiuDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. Liu.Yuanhang@mayo.edu.
Hui TangDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. Tang.Hui@mayo.edu.
Kyra L JordanDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. Jordan.Kyra@mayo.edu.
Lilach O LermanDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. Lerman.Lilach@mayo.edu.ORCID 0000-0002-3271-3887
Alfonso EirinDepartment of Internal Medicine, Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN 55905, USA. eirinmassat.alfonso@mayo.edu.
Mayo Clinic · US

Funding

MSC-derived microvesicles in metabolic syndrome and renovascular diseaseR01DK102325 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2015 to 2018
$2.8M
Obesity-induced mesenchymal stem cell senescenceR01DK120292 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2019 to 2022
$2.6M
Noninvasive assessment of renal fibrosis using magnetization transfer MRIU01DK104273 · NIDDK · MAYO CLINIC ROCHESTER · PI LERMAN, LILACH O · 2014 to 2018
$1.8M
A potential role for mitoprotection in preserving the kidney in metabolic syndrome and renal artery stenosisK08DK106427 · NIDDK · MAYO CLINIC ROCHESTER · PI EIRIN, ALFONSO · 2015 to 2019
$819k
Mitochondrial injury interferes with endogenous renal repair in experimental renovascular diseaseR03DK122137 · NIDDK · MAYO CLINIC ROCHESTER · PI EIRIN, ALFONSO · 2019 to 2020
$239k
NIDDK NIH HHS DK102325NIDDK NIH HHS DK104273NIDDK NIH HHS DK106427NIDDK NIH HHS DK120292NIDDK NIH HHS DK122137NIDDK NIH HHS K08 DK106427NIDDK NIH HHS R03 DK122137NIDDK NIH HHS U01 DK104273
6 · The paper itself

Abstract

backgroundScattered tubular-like cells (STCs) proliferate and differentiate to support neighboring injured renal tubular cells during recovery from insults. Renal artery stenosis (RAS) induces renal ischemia and hypertension and leads to loss of kidney function, but whether RAS alters renal endogenous repair mechanisms, such as STCs, remains unknown. We hypothesize that RAS in swine modifies the messenger RNA (mRNA) profile of STCs, blunting their in vitro reparative capacity.

methodsCD24+/CD133+ STCs were isolated from pig kidneys after 10-weeks of RAS or sham (

resultsOf all expressed genes, 1430 genes were upregulated and 315 downregulated in RAS- versus Normal-STCs. Expression of selected candidate genes followed the same fold change directions as the mRNAseq findings. Genes upregulated in RAS-STCs were involved in cell adhesion, extracellular matrix remodeling, and kidney development, whereas those downregulated in RAS-STCs are related to cell cycle and cytoskeleton. The percentage of STCs from dissociated kidney cells was higher in RAS versus Normal pigs, but their proliferation rate was blunted.

conclusionsRenal ischemia and hypertension in swine induce changes in the mRNA profile of STCs, associated with increased STC activation and impaired proliferation. These observations suggest that RAS may alter the reparative capacity of STCs.

Indexed as

TranscriptomeAnimalsCells, CulturedFemaleKidney TubulesRenal Artery ObstructionSwinehypertensionmRNA sequencingrenal artery stenosisscattered tubular-like cells

Identifiers

PMID31614781
PMCPMC6829501
OpenAlexW2979897136

What OpenQuestion holds

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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 OpenQuestion graph.