Evidence map›Paper›PMID 36705802›Full record

ReviewReviews in endocrine & metabolic disorders2023

Mitochondrial epigenetic modifications and nuclear-mitochondrial communication: A new dimension towards understanding and attenuating the pathogenesis in women with PCOS.

Pallavi Shukla, Girish C Melkani

Open access · greenAbstract readReview
In one paragraph

Review in Reviews in endocrine & metabolic disorders, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Evolving PCOS Management: From Symptom Control to Phenotype-Targeted Therapy.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
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

2 authors at 2 institutions in 2 countries.

Pallavi ShuklaDepartment of Molecular Endocrinology, Indian Council of Medical Research-National Institute for Research in Reproductive and Child Health (ICMR-NIRRCH), J.M. Street, Parel, Mumbai, 400012, India. shuklap@nirrch.res.in.
Girish C MelkaniDepartment of Pathology, Division of Molecular and Cellular Pathology, Heersink School of Medicine, University of Alabama at Birmingham, Birmingham, AL, 35294, United States.
Indian Council of Medical Research · INUniversity of Alabama at Birmingham · US

Funding

Molecular basis of circadian rhythms disruptions linked cardiometabolic disorders and their mitigation using dietary interventionR01AG065992 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MELKANI, GIRISH C. · 2019 to 2023
$1.9M
NIA NIH HHS R01 AG065992
6 · The paper itself

Abstract

Mitochondrial DNA (mtDNA) epigenetic modifications have recently gained attention in a plethora of complex diseases, including polycystic ovary syndrome (PCOS), a common cause of infertility in women of reproductive age. Herein we discussed mtDNA epigenetic modifications and their impact on nuclear-mitochondrial interactions in general and the latest advances indicating the role of mtDNA methylation in the pathophysiology of PCOS. We highlighted epigenetic changes in nuclear-related mitochondrial genes, including nuclear transcription factors that regulate mitochondrial function and may be involved in the development of PCOS or its related traits. Additionally, therapies targeting mitochondrial epigenetics, including time-restricted eating (TRE), which has been shown to have beneficial effects by improving mitochondrial function and may be mediated by epigenetic modifications, have also been discussed. As PCOS has become a major metabolic disorder and a risk factor for obesity, cardiometabolic disorders, and diabetes, lifestyle/behavior intervention using TRE that reinforces feeding-fasting rhythms without reducing caloric intake may be a promising therapeutic strategy for attenuating the pathogenesis. Furthermore, future perspectives in the area of mitochondrial epigenetics are described.

Indexed as

Polycystic Ovary SyndromeCommunicationDNA, MitochondrialEpigenesis, GeneticFemaleHumansMitochondriaDNA, MitochondrialEpigenetic modificationsMitochondrial DNAMitochondrial dysfunctionNuclear mitochondrial communicationPolycystic ovary syndromeTime-restricted eating

Identifiers

PMID36705802
PMCPMC10150397
OpenAlexW4318263628

What OpenQuestion holds

Textmetadata
LicenceTDM
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.