Evidence mapPaperPMID 36010613Full record

ArticleCells2022

New Insights on the Regulation of the Insulin-Degrading Enzyme: Role of microRNAs and RBPs.

Yolanda Martín-Martín, Ana Pérez-García, Marta Torrecilla-Parra, Mario Fernández-de Frutos, Virginia Pardo-Marqués, María José Casarejos, Rebeca Busto, Cristina M Ramírez

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

7 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Yolanda Martín-MartínIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
Ana Pérez-GarcíaIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
Marta Torrecilla-ParraIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
Mario Fernández-de FrutosIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
Virginia Pardo-MarquésIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
María José CasarejosServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), Hospital Universitario Ramón y Cajal, 28034 Madrid, Spain.
Rebeca BustoServicio de Bioquímica-Investigación, Hospital Universitario Ramón y Cajal, IRYCIS, 28034 Madrid, Spain.ORCID 0000-0001-9869-4087
Cristina M RamírezIMDEA Research Institute of Food and Health Sciences, 28049 Madrid, Spain.
IMDEA Food · ESInstituto Ramón y Cajal de Investigación Sanitaria · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evident implication of the insulin-degrading enzyme (IDE) in Alzheimer's disease (AD) and type 2 diabetes mellitus (T2DM), among its capacity to degrade insulin and amyloid-β peptide (Aβ), suggests that IDE could be an essential link in the relation between hyperinsulinemia, insulin resistance and AD. However, little is known about the cellular and molecular regulation of IDE expression, and even less has been explored regarding the post-transcriptional regulation of IDE, although it represents a great molecular target of interest for therapeutic treatments. We recently described that miR-7, a novel candidate for linking AD and T2DM at the molecular level, regulates IDE and other key genes in both pathologies, including some key genes involved in the insulin signaling pathway. Here, we explored whether other miRNAs as well as other post-transcriptional regulators, such as RNA binding proteins (RBP), could potentially participate in the regulation of IDE expression in vitro. Our data showed that in addition to miR-7, miR-125, miR-490 and miR-199 regulate IDE expression at the post-transcriptional level. Moreover, we also found that IDE contains multiple potential binding sites for several RBPs, and a narrow-down prediction analysis led us to speculate on a novel regulation of IDE by RALY and HuD. Taken together, these results demonstrate the novel players controlling IDE expression that could represent potential therapeutical targets to treat several metabolic diseases with a high impact on human health, including AD and T2DM.

Indexed as

Alzheimer DiseaseDiabetes Mellitus, Type 2InsulysinMicroRNAsAmyloid beta-PeptidesHeterogeneous-Nuclear Ribonucleoprotein Group CHumansInsulinAmyloid beta-PeptidesHeterogeneous-Nuclear Ribonucleoprotein Group CInsulinInsulysinMicroRNAsRALY protein, humanAlzheimer’s disease (AD)diabetesinsulininsulin-degrading enzyme (IDE)RNA binding proteins (RBPs)

Identifiers

PMID36010613
PMCPMC9406717
OpenAlexW4292291545

What Socratic holds

Textmetadata
LicenceCC BY
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.