Evidence map›Paper›PMID 32992734›Full record

ReviewInternational journal of molecular sciences2020

In Search of New Therapeutics-Molecular Aspects of the PCOS Pathophysiology: Genetics, Hormones, Metabolism and Beyond.

Agata Wawrzkiewicz-Jałowiecka, Karolina Kowalczyk, Paulina Trybek, Tomasz Jarosz, Patrycja Radosz, Marcin Setlak, Paweł Madej

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
8.2field-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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 citations in OpenAlex.

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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

7 authors at 3 institutions in 1 country.

Agata Wawrzkiewicz-JałowieckaDepartment of Physical Chemistry and Technology of Polymers, Silesian University of Technology, 44-100 Gliwice, Poland.ORCID 0000-0001-6885-3956
Karolina KowalczykDepartment of Obstetrics and Gynecology, Medical University of Silesia in Katowice, 40-752 Katowice, Poland.ORCID 0000-0003-1406-5211
Paulina TrybekFaculty of Science and Technology, University of Silesia in Katowice, 41-500 Chorzow, Poland.
Tomasz JaroszDepartment of Physical Chemistry and Technology of Polymers, Silesian University of Technology, 44-100 Gliwice, Poland.ORCID 0000-0001-8870-3760
Patrycja RadoszDepartment of Obstetrics and Gynecology, Medical University of Silesia in Katowice, 40-752 Katowice, Poland.
Marcin SetlakDepartment of Neurosurgery, Medical University of Silesia, 40-752 Katowice, Poland.
Paweł MadejDepartment of Obstetrics and Gynecology, Medical University of Silesia in Katowice, 40-752 Katowice, Poland.ORCID 0000-0002-6447-1667
Medical University of Silesia · PLSilesian University of Technology · PLUniversity of Silesia in Katowice · PL

Funding

Politechnika Śląska BKM-528/RCh4/2020
6 · The paper itself

Abstract

In a healthy female reproductive system, a subtle hormonal and metabolic dance leads to repetitive cyclic changes in the ovaries and uterus, which make an effective ovulation and potential implantation of an embryo possible. However, that is not so in the case of polycystic ovary syndrome (PCOS), in which case the central mechanism responsible for entraining hormonal and metabolic rhythms during the menstrual cycle is notably disrupted. In this review we provide a detailed description of the possible scenario of PCOS pathogenesis. We begin from the analysis of how a set of genetic disorders related to PCOS leads to particular malfunctions at a molecular level (e.g., increased enzyme activities of cytochrome P450 (CYP) type 17A1 (17α-hydroxylase), 3β-HSD type II and CYP type 11A1 (side-chain cleavage enzyme) in theca cells, or changes in the expression of aquaporins in granulosa cells) and discuss further cellular- and tissue-level consequences (e.g., anovulation, elevated levels of the advanced glycation end products in ovaries), which in turn lead to the observed subsequent systemic symptoms. Since gene-editing therapy is currently out of reach, herein special emphasis is placed on discussing what kinds of drug targets and which potentially active substances seem promising for an effective medication, acting on the primary causes of PCOS on a molecular level.

Indexed as

Polycystic Ovary Syndrome3-Hydroxysteroid DehydrogenasesAquaporinsCholesterol Side-Chain Cleavage EnzymeFemaleGranulosa CellsHormonesHumansSteroid 17-alpha-HydroxylaseTheca Cells3-Hydroxysteroid DehydrogenasesAquaporinsCholesterol Side-Chain Cleavage EnzymeCYP17A1 protein, humanHormonesSteroid 17-alpha-HydroxylaseAQPs-oriented therapyberberineGABAinositolskisspeptinmolecular mechanismnaringeninnovel therapiespolycystic ovary syndrome (PCOS)

Identifiers

PMID32992734
PMCPMC7582580
OpenAlexW3088685410

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.