Evidence map›Paper›PMID 25950485›Full record

ArticleCell death & disease2015

Mcl-1 is a key regulator of the ovarian reserve.

S Omari, M Waters, T Naranian, K Kim, A L Perumalsamy, M Chi, E Greenblatt, K H Moley, J T Opferman, A Jurisicova

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Selected Genetic Factors Associated with Primary Ovarian Insufficiency.International journal of molecular sciences · 2023
    Review
  11. Regulation of Oocyte Apoptosis: A View from Gene Knockout Mice.International journal of molecular sciences · 2023
    Review
  12. Aging conundrum: A perspective for ovarian aging.Frontiers in endocrinology · 2022
    Review
  13. Review
  14. Physiological Functions of Mcl-1: Insights From Genetic Mouse Models.Frontiers in cell and developmental biology · 2021
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Autophagy in Ovarian Follicular Development and Atresia.International journal of biological sciences · 2019
    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

10 authors at 5 institutions in 2 countries.

S Omari1] Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada [2] Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.
M WatersLunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada.
T Naranian1] Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada [2] Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.
K Kim1] Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada [2] Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada.
A L PerumalsamyLunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada.
M ChiDepartment of Obstetrics and Gynecology, Washington University in St. Louis, 660S Euclid Avenue, St. Louis, MO 63110, USA.
E Greenblatt1] Centre for Fertility and Reproductive Health, Mount Sinai Hospital, 250 Dundas Street, Toronto, Ontario M5T 2Z5, Canada [2] Department of Obstetrics and Gynecology, University of Toronto, 92 College Street, Toronto, Ontario M5G 1L4, Canada.
K H MoleyDepartment of Obstetrics and Gynecology, Washington University in St. Louis, 660S Euclid Avenue, St. Louis, MO 63110, USA.
J T OpfermanDepartment of Biochemistry, St. Jude Children's Research Hospital, MS 340, Room D4063D, 262 Danny Thomas Place, Memphis, TN 38105, USA.
A Jurisicova1] Lunenfeld Tanenbaum Research Institute, Mount Sinai Hospital, 25 Orde Street, Toronto, Ontario M5T 3H7, Canada [2] Department of Physiology, University of Toronto, 1 King's College Circle, Toronto, Ontario M5S 1A8, Canada [3] Department of Obstetrics and Gynecology, University of Toronto, 92 College Street, Toronto, Ontario M5G 1L4, Canada.
Lunenfeld-Tanenbaum Research Institute · CAMount Sinai Hospital · CAWashington University in St. Louis · USSt. Jude Children's Research Hospital · USUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research FRN 123518
6 · The paper itself

Abstract

A majority of ovarian follicles are lost to natural death, but the disruption of factors involved in maintenance of the oocyte pool results in a further untimely follicular depletion known as premature ovarian failure. The anti-apoptotic B-cell lymphoma 2 (Bcl-2) family member myeloid cell leukemia-1 (MCL-1) has a pro-survival role in various cell types; however, its contribution to oocyte survival is unconfirmed. We present a phenotypic characterization of oocytes deficient in Mcl-1, and establish its role in maintenance of the primordial follicle (PMF) pool, growing oocyte survival and oocyte quality. Mcl-1 depletion resulted in the premature exhaustion of the ovarian reserve, characterized by early PMF loss because of activation of apoptosis. The increasingly diminished surviving cohort of growing oocytes displayed elevated markers of autophagy and mitochondrial dysfunction. Mcl-1-deficient ovulated oocytes demonstrated an increased susceptibility to cellular fragmentation with activation of the apoptotic cascade. Concomitant deletion of the pro-apoptotic Bcl-2 member Bcl-2-associated X protein (Bax) rescued the PMF phenotype and ovulated oocyte death, but did not prevent the mitochondrial dysfunction associated with Mcl-1 deficiency and could not rescue long-term breeding performance. We thus recognize MCL-1 as the essential survival factor required for conservation of the postnatal PMF pool, growing follicle survival and effective oocyte mitochondrial function.

Indexed as

AnimalsApoptosisFemaleHumansMiceMice, TransgenicMyeloid Cell Leukemia Sequence 1 ProteinOocytesOvarian ReserveMCL1 protein, humanMcl1 protein, mouseMyeloid Cell Leukemia Sequence 1 Protein

Identifiers

PMID25950485
PMCPMC4669721
OpenAlexW2111299532

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.