Evidence map›Paper›PMID 30208759›Full record

ReviewAutophagy2019

How does estrogen work on autophagy?

Jin Xiang, Xiang Liu, Jing Ren, Kun Chen, Hong-Lu Wang, Yu-Yang Miao, Miao-Miao Qi

Open access · bronzeAbstract readReview
In one paragraph

Review in Autophagy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

66 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  15. Frontiers in veterinary science · 2025
    Article
  16. Review
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  19. Review
  20. Article

6 more citing papers are in PubMed but not listed here.

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

7 authors at 1 institution in 1 country.

Jin Xianga Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Xiang Liua Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Jing Rena Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Kun Chena Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Hong-Lu Wanga Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Yu-Yang Miaoa Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Miao-Miao Qia Key Laboratory of Combinatorial Biosynthesis and Drug Discovery, Ministry of Education, School of Pharmaceutical Sciences , Wuhan University , Wuhan , PR China.
Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macroautophagy/autophagy is vital for intracellular quality control and homeostasis. Therefore, careful regulation of autophagy is very important. In the past 10 years, a number of studies have reported that estrogenic effectors affect autophagy. However, some results, especially those regarding the modulatory effect of 17β-estradiol (E2) on autophagy seem inconsistent. Moreover, several clinical trials are already in place combining both autophagy inducers and autophagy inhibitors with endocrine therapies for breast cancer. Not all patients experience benefit, which further confuses and complicates our understanding of the main effects of autophagy in estrogen-related cancer. In view of the importance of the crosstalk between estrogen signaling and autophagy, this review summarizes the estrogenic effectors reported to affect autophagy, subcellular distribution and translocation of estrogen receptors, autophagy-targeted transcription factors (TFs), miRNAs, and histone modifications regulated by E2. Upon stimulation with estrogen, there will always be opposing functional actions, which might occur between different receptors, receptors on TFs, TFs on autophagy genes, or even histone modifications on transcription. The huge signaling network downstream of estrogen can promote autophagy and reduce overstimulated autophagy at the same time, which allows autophagy to be regulated by estrogen in a restricted range. To help understand how the estrogenic regulation of autophagy affects cell fate, a hypothetical model is presented here. Finally, we discuss some exciting new directions in the field. We hope this might help to better understand the multiple associations between estrogen and autophagy, the pathogenic mechanisms of many estrogen-related diseases, and to design novel and efficacious therapeutics.

Indexed as

AutophagyAnimalsEstrogensHistonesHumansMicroRNAsReceptors, EstrogenTranscription FactorsEstrogensHistonesMicroRNAsReceptors, EstrogenTranscription FactorsAutophagycancercell homeostasisestrogenhistone modificationsmiRNAsreceptors of estrogenTFs

Identifiers

PMID30208759
PMCPMC6333457
OpenAlexW2890763920

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.