Evidence map›Paper›PMID 36077083›Full record

ReviewInternational journal of molecular sciences2022

Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?

Ekaterina M Zhidkova, Evgeniya S Lylova, Diana D Grigoreva, Kirill I Kirsanov, Alena V Osipova, Evgeny P Kulikov, Sergey A Mertsalov, Gennady A Belitsky, Irina Budunova, Marianna G Yakubovskaya and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. 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
3.3field-weighted citation impact, top 6% 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, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Nomilin Rewires mTOR-Driven Immunometabolism via DDIT4 to Restrain Psoriasis.International journal of biological sciences · 2026
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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

11 authors at 3 institutions in 2 countries.

Ekaterina M ZhidkovaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.ORCID 0000-0003-3318-9391
Evgeniya S LylovaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.
Diana D GrigorevaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.
Kirill I KirsanovDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.ORCID 0000-0002-8599-6833
Alena V OsipovaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.
Evgeny P KulikovFaculty of Oncology, I.P. Pavlov Ryazan State Medical University, 390026 Ryazan, Russia.
Sergey A MertsalovFaculty of Oncology, I.P. Pavlov Ryazan State Medical University, 390026 Ryazan, Russia.
Gennady A BelitskyDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.
Irina BudunovaDepartment of Dermatology, Northwestern University, Chicago, IL 60611, USA.ORCID 0000-0001-5880-6822
Marianna G YakubovskayaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.ORCID 0000-0002-9710-8178
Ekaterina A LesovayaDepartment of Chemical Carcinogenesis, N.N. Blokhin NMRCO, 115478 Moscow, Russia.ORCID 0000-0002-1967-9637
Ryazan State Medical University named after Academician I.P. Pavlov · RUNorthwestern University · USPeoples' Friendship University of Russia · RU

Funding

REDD1 dissociates the therapeutic and adverse effects of glucocorticoids in skinR01AI125366 · NIAID · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BUDUNOVA, IRINA · 2017 to 2021
$2.4M
Integrative informatics approach to develop safe glucocorticoid therapiesR01GM112945 · NIGMS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BUDUNOVA, IRINA, MA'AYAN, AVI · 2015 to 2018
$2.1M
NIAID NIH HHS R01 AI125366NIGMS NIH HHS R01 GM112945Russian Science Foundation 17-75-20124
6 · The paper itself

Abstract

Regulated in Development and DNA Damage Response 1 (REDD1)/DNA Damage-Induced Transcript 4 (DDIT4) is an immediate early response gene activated by different stress conditions, including growth factor depletion, hypoxia, DNA damage, and stress hormones, i.e., glucocorticoids. The most known functions of REDD1 are the inhibition of proliferative signaling and the regulation of metabolism via the repression of the central regulator of these processes, the mammalian target of rapamycin (mTOR). The involvement of REDD1 in cell growth, apoptosis, metabolism, and oxidative stress implies its role in various pathological conditions, including cancer and inflammatory diseases. Recently, REDD1 was identified as one of the central genes mechanistically involved in undesirable atrophic effects induced by chronic topical and systemic glucocorticoids widely used for the treatment of blood cancer and inflammatory diseases. In this review, we discuss the role of REDD1 in the regulation of cell signaling and processes in normal and cancer cells, its involvement in the pathogenesis of different diseases, and the approach to safer glucocorticoid receptor (GR)-targeted therapies via a combination of glucocorticoids and REDD1 inhibitors to decrease the adverse atrophogenic effects of these steroids.

Indexed as

GlucocorticoidsNeoplasmsHumansInflammationReceptors, GlucocorticoidSignal TransductionTranscription FactorsDDIT4 protein, humanGlucocorticoidsReceptors, GlucocorticoidTranscription Factorscancercombination therapyglucocorticoidsinflammationmetabolismmTORREDD1

Identifiers

PMID36077083
PMCPMC9456073
OpenAlexW4293536203

What OpenQuestion 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 OpenQuestion graph.