Evidence map›Paper›PMID 30695997›Full record

ReviewCells2019

Autophagy: Dual Response in the Development of Hepatocellular Carcinoma.

Hamza O Yazdani, Hai Huang, Allan Tsung

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
9.3field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
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  11. [Research progress on the mechanism of action of mitophagy in the occurrence and development of liver cancer].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023
    Review
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  18. Marine drugs · 2022
    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

3 authors at 2 institutions in 1 country.

Hamza O YazdaniDepartment of Surgery, University of Pittsburgh, Pittsburg, PA 15213-2582, USA. obaidh3@upmc.edu.ORCID 0000-0002-3437-0339
Hai HuangDivision of Surgical Oncology, Department of Surgery, The Ohio State University Wexner Medical Center, N924 Doan Hall, 410 West 10th Ave., Columbus, OH 43210, USA. huang.3900@osu.edu.
Allan TsungDivision of Surgical Oncology, Department of Surgery, The Ohio State University Wexner Medical Center, N924 Doan Hall, 410 West 10th Ave., Columbus, OH 43210, USA. Allan.Tsung@osumc.edu.
The Ohio State University Wexner Medical Center · USUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionary conserved intracellular mechanism which helps eukaryotic cells in maintaining their metabolic state to afford high-efficiency energy requirements. In the physiology of a normal liver and the pathogenesis of liver diseases, autophagy plays a crucial role. Autophagy has been found to be both upregulated and downregulated in different cancers providing the evidence that autophagy plays a dual role in suppressing and promoting cell survival. Hepatocellular carcinoma (HCC) is the most common primary liver cancer and the major leading cause of cancer mortality worldwide. In light of its high complexity and poor prognosis, it is essential to improve our understanding of autophagy's role in HCC. In this review, we summarize the dual mechanism of autophagy in the development of HCC and elucidate the currently used therapeutic strategies for anti-HCC therapy.

Indexed as

AutophagyCarcinoma, HepatocellularHomeostasisHumansLiverLiver NeoplasmsNeoplasm MetastasisHCC therapyhepatocellular carcinomainflammationmitophagyoxidative stress

Identifiers

PMID30695997
PMCPMC6406383
OpenAlexW2913162269

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.