Evidence map›Paper›PMID 31393557›Full record

ReviewEndocrinology2019

Mitochondrial Dysfunction in Primary Ovarian Insufficiency.

Dov Tiosano, Jason A Mears, David A Buchner

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
2.8field-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

65 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. [HeZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2025
    Article
  10. Article
  11. Sirtuins in Women's Health.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. The mitochondrial DNA copy number and ovary-related reproductive disorders: A bidirectional two-sample Mendelian randomization study.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2025
    Article

5 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

3 authors at 2 institutions in 2 countries.

Dov TiosanoDivision of Pediatric Endocrinology, Ruth Rappaport Children's Hospital, Rambam Medical Center, Haifa, Israel.
Jason A MearsCenter for Mitochondrial Diseases, Case Western Reserve University, Cleveland, Ohio.
David A BuchnerDepartment of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, Ohio.
Case Western Reserve University · USTechnion – Israel Institute of Technology · IL

Funding

Supplement: Defining Molecular Interactions that Drive Mitochondrial FissionR01GM125844 · NIGMS · CASE WESTERN RESERVE UNIVERSITY · PI Jason Mears · 2018 to 2026
$2.8M
Role of adipocyte gene expression regulation by Zfp407 in adipocyte biology and metabolic diseaseR01DK119305 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BUCHNER, DAVID A · 2019 to 2023
$2.0M
Mitochondrial Dynamics in Brain TumorInitiating CellsR01CA208516 · NCI · CASE WESTERN RESERVE UNIVERSITY · PI MEARS, JASON · 2017 to 2021
$1.6M
Molecular regulation of PPARg signaling and adipocyte functionR56DK112846 · NIDDK · CASE WESTERN RESERVE UNIVERSITY · PI BUCHNER, DAVID A · 2017 to 2017
$400k
NCI NIH HHS R01 CA208516NIDDK NIH HHS R01 DK119305NIDDK NIH HHS R56 DK112846NIGMS NIH HHS R01 GM125844
6 · The paper itself

Abstract

Primary ovarian insufficiency (POI) is defined by the loss or dysfunction of ovarian follicles associated with amenorrhea before the age of 40. Symptoms include hot flashes, sleep disturbances, and depression, as well as reduced fertility and increased long-term risk of cardiovascular disease. POI occurs in ∼1% to 2% of women, although the etiology of most cases remains unexplained. Approximately 10% to 20% of POI cases are due to mutations in a single gene or a chromosomal abnormality, which has provided considerable molecular insight into the biological underpinnings of POI. Many of the genes for which mutations have been associated with POI, either isolated or syndromic cases, function within mitochondria, including MRPS22, POLG, TWNK, LARS2, HARS2, AARS2, CLPP, and LRPPRC. Collectively, these genes play roles in mitochondrial DNA replication, gene expression, and protein synthesis and degradation. Although mutations in these genes clearly implicate mitochondrial dysfunction in rare cases of POI, data are scant as to whether these genes in particular, and mitochondrial dysfunction in general, contribute to most POI cases that lack a known etiology. Further studies are needed to better elucidate the contribution of mitochondria to POI and determine whether there is a common molecular defect in mitochondrial function that distinguishes mitochondria-related genes that when mutated cause POI vs those that do not. Nonetheless, the clear implication of mitochondrial dysfunction in POI suggests that manipulation of mitochondrial function represents an important therapeutic target for the treatment or prevention of POI.

Indexed as

FemaleGene Expression RegulationHumansInfertility, FemaleMitochondrial DiseasesPrimary Ovarian Insufficiency

Identifiers

PMID31393557
PMCPMC6760336
OpenAlexW2968053316

What OpenQuestion holds

Textmetadata
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.