Evidence map›Paper›PMID 28815060›Full record

ArticleCell death discovery2017

Defective expression of ATG4D abrogates autophagy and promotes growth in human uterine fibroids.

Abdeljabar El Andaloussi, Samar Habib, Gizem Soylemes, Archana Laknaur, Heba Elhusseini, Ayman Al-Hendy, Nahed Ismail

Open access · goldAbstract read
In one paragraph

Article in Cell death discovery, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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  5. Article
  6. Review
  7. Article
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  14. RNA sequence analysis of nasopharyngeal swabs from asymptomatic and mildly symptomatic patients with COVID-19.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022
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  15. Review
  16. The Multifaceted Role of Autophagy in Endometrium Homeostasis and Disease.Reproductive sciences (Thousand Oaks, Calif.) · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Molecular basis of reproductive senescence: insights from model organisms.Journal of assisted reproduction and genetics · 2021
    Review
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 2 institutions in 1 country.

Abdeljabar El AndaloussiDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Samar HabibDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Gizem SoylemesDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Archana LaknaurDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Heba ElhusseiniDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Ayman Al-HendyDepartment of Obstetrics and Gynecology, Medical College of Georgia, Augusta University, Augusta, GA, USA.
Nahed IsmailClinical Microbiology Division, Department of Pathology, University of Pittsburgh, Pittsburgh, PA, USA.
Augusta University · USUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uterine fibroids (UF) are the most common pelvic tumors in women of reproductive-age and they usually cause heavy menstrual bleeding, pain and infertility. Autophagy is a collection of processes that enables the cells to digest and recycle their cytoplasmic contents, such as toxic protein aggregates, defunct or disused organelles and invading microorganisms. Dysregulation in autophagy process were described in neoplasms; however, the contribution of autophagy to the pathogenesis of UF remains unknown. In this study, we demonstrate that autophagy is deregulated in human UF as evidenced by significant accumulation of autophagosome in human UF cells compared to normal myometrium cells. Analysis of the autophagy markers revealed an enhanced initiation of the autophagy in UF tissues compared to their adjacent myometrial tissues (MyoF). However, autophagosome maturation and flux was blocked in UF tissues, as marked by accumulation of LC3-B and P62 protein. This block was associated with defective expression of autophagy-related protein 4 (ATG4) in the UF tissues compared to MyoF in ~90% of patient samples. Silencing of ATG4D in normal human myometrial cells resulted in defective autophagy flux, enhanced cell proliferation and increased extracellular matrix production, which phenocopy UF cell line. This study indicates that impairment of autophagy flux secondary to defective expression of ATG4D expression is a new mechanistic aberration that contributes to UF pathogenesis. Targeting autophagy pathway could provide novel medical therapeutic approach for non-surgical treatment of UF.

Identifiers

PMID28815060
PMCPMC5554887
OpenAlexW2749644107

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.