Evidence map›Paper›PMID 22160220›Full record

ArticleMolecular medicine (Cambridge, Mass.)2012

Insulin receptor substrate 2 (IRS2)-deficient mice show sensorineural hearing loss that is delayed by concomitant protein tyrosine phosphatase 1B (PTP1B) loss of function.

Silvia Murillo-Cuesta, Guadalupe Camarero, Agueda González-Rodríguez, Lourdes Rodríguez De La Rosa, Deborah J Burks, Carlos Avendaño, Angela M Valverde, Isabel Varela-Nieto

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  14. C-Raf deficiency leads to hearing loss and increased noise susceptibility.Cellular and molecular life sciences : CMLS · 2015
    Article
  15. Folic acid deficiency induces premature hearing loss through mechanisms involving cochlear oxidative stress and impairment of homocysteine metabolism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015
    Article
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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 6 institutions in 1 country.

Silvia Murillo-CuestaInstitute of Biomedical Research "Alberto Sols" (IIBM), Spanish National Research Council-Autonomous University of Madrid-CSIC-UAM, Madrid, Spain. smurillo@iib.uam.es
Guadalupe Camarero
Agueda González-Rodríguez
Lourdes Rodríguez De La Rosa
Deborah J Burks
Carlos Avendaño
Angela M Valverde
Isabel Varela-Nieto
Instituto de Investigaciones Biomédicas Sols-Morreale · ESUniversidad Autónoma de Madrid · ESCentre for Biomedical Network Research on Rare Diseases · ESConsejo Superior de Investigaciones Científicas · ESHospital La Paz Institute for Health Research · ESSpanish Biomedical Research Centre in Physiopathology of Obesity and Nutrition · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The insulin receptor substrate (IRS) proteins are key mediators of insulin and insulinlike growth factor 1 (IGF-1) signaling. Protein tyrosine phosphatase (PTP)-1B dephosphorylates and inactivates both insulin and IGF-1 receptors. IRS2-deficient mice present altered hepatic insulin signaling and β-cell failure and develop type 2-like diabetes. In addition, IRS2 deficiency leads to developmental defects in the nervous system. IGF1 gene mutations cause syndromic sensorineural hearing loss in humans and mice. However, the involvement of IRS2 and PTP1B, two IGF-1 downstream signaling mediators, in hearing onset and loss has not been studied. Our objective was to study the hearing function and cochlear morphology of Irs2-null mice and the impact of PTP1B deficiency. We have studied the auditory brainstem responses and the cochlear morphology of systemic Irs2⁻/⁻Ptpn1⁺/⁺, Irs2⁺/⁺Ptpn1⁻/⁻ and Irs2⁻/⁻Ptpn1⁻/⁻ mice at different postnatal ages. The results indicated that Irs2⁻/⁻Ptpn1⁺/⁺ mice present a profound congenital sensorineural deafness before the onset of diabetes and altered cochlear morphology with hypoinnervation of the cochlear ganglion and aberrant stria vascularis, compared with wild-type mice. Simultaneous PTP1B deficiency in Irs2⁻/⁻Ptpn1⁻/⁻ mice delays the onset of deafness. We show for the first time that IRS2 is essential for hearing and that PTP1B inhibition may be useful for treating deafness associated with hyperglycemia and type 2 diabetes.

Indexed as

AnimalsCochleaHearing LossInsulin Receptor Substrate ProteinsMaleMiceMice, TransgenicMitogen-Activated Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Insulin Receptor Substrate ProteinsIrs2 protein, mouseMitogen-Activated Protein KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 1Ptpn1 protein, mouse

Identifiers

PMID22160220
PMCPMC3324951
OpenAlexW1608462692

What OpenQuestion 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 OpenQuestion graph.