Evidence map›Paper›PMID 32157251›Full record

ReviewNature reviews. Nephrology2020

The evolving role of TonEBP as an immunometabolic stress protein.

Soo Youn Choi, Whaseon Lee-Kwon, Hyug Moo Kwon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Nephrology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
6.0field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 85 citations in OpenAlex.

  1. Review
  2. TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026
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  18. Inhibition of NFAT5-Dependent Astrocyte Swelling Alleviates Neuropathic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Soo Youn ChoiSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.ORCID http://orcid.org/0000-0002-3149-5590
Whaseon Lee-KwonSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea.
Hyug Moo KwonSchool of Life Sciences, Ulsan National Institute of Science and Technology, Ulsan, Republic of Korea. hmkwon@unist.ac.kr.ORCID http://orcid.org/0000-0003-3244-2025
Ulsan National Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tonicity-responsive enhancer-binding protein (TonEBP), which is also known as nuclear factor of activated T cells 5 (NFAT5), was discovered 20 years ago as a transcriptional regulator of the cellular response to hypertonic (hyperosmotic salinity) stress in the renal medulla. Numerous studies since then have revealed that TonEBP is a pleiotropic stress protein that is involved in a range of immunometabolic diseases. Some of the single-nucleotide polymorphisms (SNPs) in TONEBP introns are cis-expression quantitative trait loci that affect TONEBP transcription. These SNPs are associated with increased risk of type 2 diabetes mellitus, diabetic nephropathy, inflammation, high blood pressure and abnormal plasma osmolality, indicating that variation in TONEBP expression might contribute to these phenotypes. In addition, functional studies have shown that TonEBP is involved in the pathogenesis of rheumatoid arthritis, atherosclerosis, diabetic nephropathy, acute kidney injury, hyperlipidaemia and insulin resistance, autoimmune diseases (including type 1 diabetes mellitus and multiple sclerosis), salt-sensitive hypertension and hepatocellular carcinoma. These pathological activities of TonEBP are in contrast to the protective actions of TonEBP in response to hypertonicity, bacterial infection and DNA damage induced by genotoxins. An emerging theme is that TonEBP is a stress protein that mediates the cellular response to a range of pathological insults, including excess caloric intake, inflammation and oxidative stress.

Indexed as

Arthritis, RheumatoidAtherosclerosisAutoimmune DiseasesBacterial InfectionsCarcinoma, HepatocellularDiabetes Mellitus, Type 2Diabetic NephropathiesDNA DamageHeat-Shock ProteinsHumansHyperlipidemiasHypertensionInsulin ResistanceLiver NeoplasmsNFATC Transcription FactorsObesityHeat-Shock ProteinsNFATC Transcription Factors

Identifiers

PMID32157251
OpenAlexW3011297943

What Socratic 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 Socratic graph.