Evidence map›Paper›PMID 26945277›Full record

ReviewCurrent opinion in hematology2016

The mitochondrial metabolic checkpoint and aging of hematopoietic stem cells.

Mary Mohrin, Danica Chen

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Metabolomics of healthy hematopoietic stem cells and leukemic stem cells.Journal of clinical and translational research · 2025
    Article
  3. Review
  4. Regulation of Stem Cell Function by NADPhysiology (Bethesda, Md.) · 2025
    Review
  5. Article
  6. An NADNature aging · 2024
    Article
  7. Mitochondrial regulation in stem cells.Trends in cell biology · 2024
    Review
  8. Review
  9. Review
  10. Article
  11. Stem Cell Metabolism and Diet.Current stem cell reports · 2020
    Article
  12. Review
  13. Article
  14. Regulation of stress-induced hematopoiesis.Current opinion in hematology · 2020
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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.

Mary MohrinaProgram in Metabolic Biology, Nutritional Sciences and Toxicology, University of California bCalico Life Sciences, South San Francisco, California, USA.
Danica Chen

Funding

Training in Basic Research on Aging and Age-Related DiseaseT32AG000266 · NIA · UNIVERSITY OF CALIF-LAWRENC BERKELEY LAB · PI Lisa M Ellerby · 1998 to 2026
$13.8M
Nutrient Sensing and the Oxidative Stress ResponseR01AG040990 · NIA · UNIVERSITY OF CALIFORNIA BERKELEY · PI CHEN, DANICA · 2011 to 2015
$1.5M
Obesity and HematopoiesisR01DK101885 · NIDDK · UNIVERSITY OF CALIFORNIA BERKELEY · PI CHEN, DANICA · 2015 to 2017
$942k
NIA NIH HHS R01 AG040990NIA NIH HHS T32 AG000266NIDDK NIH HHS R01 DK101885
6 · The paper itself

Abstract

purpose of reviewCell-cycle checkpoints are surveillance mechanisms in eukaryotic cells that monitor the condition of the cell, repair cellular damages, and allow the cell to progress through the various phases of the cell cycle when conditions become favorable. We review recent advances in hematopoietic stem cell (HSC) biology, highlighting a mitochondrial metabolic checkpoint that is essential for HSCs to return to the quiescent state. RECENT

findingsAs quiescent HSCs enter the cell cycle, mitochondrial biogenesis is induced, which is associated with increased mitochondrial protein folding stress and mitochondrial oxidative stress. Mitochondrial unfolded protein response and mitochondrial oxidative stress response are activated to alleviate stresses and allow HSCs to exit the cell cycle and return to quiescence. Other mitochondrial maintenance mechanisms include mitophagy and asymmetric segregation of aged mitochondria. SUMMARY: Because loss of HSC quiescence results in the depletion of the HSC pool and compromised tissue regeneration, deciphering the molecular mechanisms that regulate the mitochondrial metabolic checkpoint in HSCs will increase our understanding of hematopoiesis and how it becomes dysregulated under pathological conditions and during aging. More broadly, this knowledge is instrumental for understanding the maintenance of cells that convert between quiescence and proliferation to support their physiological functions.

Indexed as

Cell Cycle CheckpointsCellular SenescenceEnergy MetabolismAnimalsGene Expression RegulationHematopoietic Stem CellsHumansMitochondriaMitophagyOxidative StressSignal TransductionUnfolded Protein Response

Identifiers

PMID26945277
PMCPMC4891268
OpenAlexW2314047536

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.