Evidence map›Paper›PMID 33462216›Full record

ArticleNature communications2021

Loss of POMC-mediated antinociception contributes to painful diabetic neuropathy.

Divija Deshpande, Nitin Agarwal, Thomas Fleming, Claire Gaveriaux-Ruff, Christoph S N Klose, Anke Tappe-Theodor, Rohini Kuner, Peter Nawroth

Erratum issuedOpen access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

14 citing papers in PubMed, 25 citations in OpenAlex.

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  14. MeCP2 Epigenetic Silencing ofFrontiers in neuroscience · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Divija DeshpandeDepartment of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany.
Nitin Agarwal *Institute of Pharmacology, Heidelberg University, INF 366, Heidelberg, 69120, Germany.
Thomas Fleming *Department of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany.
Claire Gaveriaux-RuffInstitut de Génétique et de Biologie Moléculaire et Cellulaire, Department of Translational Medicine and Neurogenetics, Illkirch, France.ORCID http://orcid.org/0000-0002-3523-8102
Christoph S N KloseDepartment of Microbiology, Infectious Diseases and Immunology, Charité -Universitätsmedizin Berlin, Hindenburgdamm 30, 12203, Berlin, Germany.ORCID http://orcid.org/0000-0001-8803-2979
Anke Tappe-TheodorInstitute of Pharmacology, Heidelberg University, INF 366, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-9343-7580
Rohini KunerInstitute of Pharmacology, Heidelberg University, INF 366, Heidelberg, 69120, Germany.ORCID http://orcid.org/0000-0002-3333-9129
Peter NawrothDepartment of Medicine I and Clinical Chemistry, University Hospital of Heidelberg, INF 410, Heidelberg, Germany. peter.nawroth@med.uni-heidelberg.de.
Heidelberg University · DECentre National de la Recherche Scientifique · FRCharité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Painful neuropathy is a frequent complication in diabetes. Proopiomelanocortin (POMC) is an endogenous opioid precursor peptide, which plays a protective role against pain. Here, we report dysfunctional POMC-mediated antinociception in sensory neurons in diabetes. In streptozotocin-induced diabetic mice the Pomc promoter is repressed due to increased binding of NF-kB p50 subunit, leading to a loss in basal POMC level in peripheral nerves. Decreased POMC levels are also observed in peripheral nervous system tissue from diabetic patients. The antinociceptive pathway mediated by POMC is further impaired due to lysosomal degradation of μ-opioid receptor (MOR). Importantly, the neuropathic phenotype of the diabetic mice is rescued upon viral overexpression of POMC and MOR in the sensory ganglia. This study identifies an antinociceptive mechanism in the sensory ganglia that paves a way for a potential therapy for diabetic neuropathic pain.

Indexed as

AgedAged, 80 and overAnimalsDiabetes Mellitus, ExperimentalDiabetic NeuropathiesFemaleGanglia, SpinalHumansLysosomesMaleMiceMice, KnockoutNociceptionPro-OpiomelanocortinProteolysisReceptors, Opioid, muOprm protein, mousePro-OpiomelanocortinReceptors, Opioid, muStreptozocin

Identifiers

PMID33462216
PMCPMC7814083
OpenAlexW3121727690

What OpenQuestion holds

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LicenceCC BY
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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.