Evidence map›Paper›PMID 33729069›Full record

ReviewScience progress

A review of the mechanism of DDIT4 serve as a mitochondrial related protein in tumor regulation.

Fadian Ding, Feng Gao, Sheng Zhang, Xiaoting Lv, Youting Chen, Qicai Liu

Open access · diamondAbstract readReview
In one paragraph

Review in Science progress. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  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

6 authors at 1 institution in 1 country.

Fadian DingDepartment of Hepatobiliary Pancreatic Surgery, 1st Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Feng GaoDepartment of Pathology, First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Sheng ZhangDepartment of Pathology, First Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Xiaoting LvDepartment of Respiratory, First Affiliated Hospital; Fujian Medical University, Fuzhou, China.ORCID 0000-0003-4100-6401
Youting ChenDepartment of Hepatobiliary Pancreatic Surgery, 1st Affiliated Hospital, Fujian Medical University, Fuzhou, China.
Qicai LiuCenter for Reproductive Medicine, First Affiliated Hospital, Fujian Medical University, Fuzhou, China.ORCID 0000-0003-1766-9395
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DDIT4 is a mitochondrial and tumor-related protein involved in anti-tumor therapy resistance, proliferation, and invasion, etc. Its expression level increases under the stress such as chemotherapy, hypoxia, and DNA damage. A number of clinical studies have confirmed that DDIT4 can change the behavior of tumor cells and the prognosis of patients with cancer. However, the role of DDIT4 in promoting or suppressing cancer is still inconclusive. This article summarized the four characteristics of DDIT4 including a mitochondria-related protein, interactions with various protein molecules, immune and metabolic cell related proteins and participator in the oxygen sensing pathway, which may be related to the progress of cancer.

Indexed as

Mitochondrial ProteinsNeoplasmsDNA DamageHumansPrognosisTranscription FactorsDDIT4 protein, humanMitochondrial ProteinsTranscription FactorsadipocytescancerDNA damage-inducible transcript 4Hypoxiaimmune

Identifiers

PMID33729069
PMCPMC10455034
OpenAlexW3136703878

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.