Evidence map›Paper›PMID 32252348›Full record

ReviewCells2020

Adipose Stromal Cell Expansion and Exhaustion: Mechanisms and Consequences.

Kristin Eckel-Mahan, Aleix Ribas Latre, Mikhail G Kolonin

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Review
  3. Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Biomarkers of aging.Science China. Life sciences · 2023
    Review
  15. Gene expression in mice with endothelium-specific telomerase knockout.Frontiers in cell and developmental biology · 2023
    Article
  16. Review
  17. Review
  18. Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Kristin Eckel-MahanInstitute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center, Houston, TX 77030, USA.
Aleix Ribas LatreHelmholtz Institute for Metabolic, Obesity and Vascular Research Center, D-04103 Leipzig, Germany.
Mikhail G KoloninInstitute of Molecular Medicine, McGovern Medical School at the University of Texas Health Science Center, Houston, TX 77030, USA.
The University of Texas Health Science Center at Houston · USHelmholtz Centre for Environmental Research · DE

Funding

Origins of Diet-Induced Circadian Reprogramming and PlasticityR01DK114037 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI MAHAN, KRISTIN ECKEL · 2018 to 2022
$1.9M
Adipose stromal cell targeting: a new approach to breast cancer treatmentR21CA216745 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI KOLONIN, MIKHAIL G, UENO, NAOTO T. · 2018 to 2019
$381k
Ablation of Non-Myogenic Progenitor Cells as a New Therapeutic Approach to Duchenne Muscular DystrophyR21AR074132 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI HUARD, JOHNNY, KOLONIN, MIKHAIL G · 2019 to 2020
$343k
NCI NIH HHS R21 CA216745NIAMS NIH HHS R21 AR074132NIDDK NIH HHS R01 DK114037
6 · The paper itself

Abstract

Adipose tissue (AT) is comprised of a diverse number of cell types, including adipocytes, stromal cells, endothelial cells, and infiltrating leukocytes. Adipose stromal cells (ASCs) are a mixed population containing adipose progenitor cells (APCs) as well as fibro-inflammatory precursors and cells supporting the vasculature. There is growing evidence that the ability of ASCs to renew and undergo adipogenesis into new, healthy adipocytes is a hallmark of healthy fat, preventing disease-inducing adipocyte hypertrophy and the spillover of lipids into other organs, such as the liver and muscles. However, there is building evidence indicating that the ability for ASCs to self-renew is not infinite. With rates of ASC proliferation and adipogenesis tightly controlled by diet and the circadian clock, the capacity to maintain healthy AT via the generation of new, healthy adipocytes appears to be tightly regulated. Here, we review the contributions of ASCs to the maintenance of distinct adipocyte pools as well as pathogenic fibroblasts in cancer and fibrosis. We also discuss aging and diet-induced obesity as factors that might lead to ASC senescence, and the consequences for metabolic health.

Indexed as

AdipocytesAdipose TissueAnimalsCell DifferentiationCircadian ClocksHumansMiceObesityStromal CellsTissue Expansionadipocyte progenitorsadipose tissuebrown adipocytescircadian clockdiabeteshyperplasiahypertrophyobesityproliferationsenescencestromal cells

Identifiers

PMID32252348
PMCPMC7226766
OpenAlexW3014668002

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.