Evidence map›Paper›PMID 34429763›Full record

ReviewOncology letters2021

Role of the CTRP family in tumor development and progression.

Mowei Kong, Yu Gao, Xiang Guo, Yuyu Xie, Yamei Yu

Abstract readReview
In one paragraph

Review in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Exploring CTRP6: a biomarker and therapeutic target in metabolic diseases.American journal of physiology. Endocrinology and metabolism · 2025
    Review
  5. Article
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  12. Article
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  15. Review
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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

5 authors.

Mowei KongDepartment of Endocrinology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Yu GaoDepartment of Endocrinology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Xiang GuoDepartment of Respiratory, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Yuyu XieDepartment of Dermatology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Yamei YuDepartment of Dermatology, Affiliated Hospital of Chengde Medical University, Chengde, Hebei 067000, P.R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C1q tumor necrosis factor-related proteins (CTRPs), which are members of the adipokine superfamily, have gained significant interest in the recent years. CTRPs are homologs of adiponectin with numerous functions and are closely associated with metabolic diseases, such as abnormal glucose and lipid metabolism and diabetes. Previous studies have demonstrated that CTRPs are highly involved in the regulation of numerous physiological and pathological processes, including glycolipid metabolism, protein kinase pathways, cell proliferation, cell apoptosis and inflammation. CTRPs also play important roles in the development and progression of numerous types of tumor, including liver, colon and lung cancers. This observation can be attributed to the fact that diabetes, obesity and insulin resistance are independent risk factors for tumorigenesis. Numerous CTRPs, including CTRP3, CTRP4, CTRP6 and CTRP8, have been reported to be associated with tumor progression by activating multiple signal pathways. CTRPs could therefore be considered as diagnostic markers and therapeutic targets in some cancers. However, the underlying mechanisms of CTRPs in tumorigenesis remain unknown. The present review aimed to determine the roles and underlying mechanisms of CTRPs in tumorigenesis, which may help the development of novel cancer treatments in the future.

Indexed as

biomarkerC1q tumor necrosis factor-related proteinmetabolismtumor

Identifiers

PMID34429763
PMCPMC8371956

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Registered trials

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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.