Evidence map›Paper›PMID 38091968›Full record

ReviewEndocrine reviews2024

Endotrophin, a Key Marker and Driver for Fibroinflammatory Disease.

Kim Henriksen, Federica Genovese, Alexander Reese-Petersen, Laurent P Audoly, Kai Sun, Morten A Karsdal, Philipp E Scherer

Open access · greenAbstract readReview
In one paragraph

Review in Endocrine reviews, 2024. 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
8.5field-weighted citation impact, top 1% 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, 35 citations in OpenAlex.

  1. Review
  2. Endotrophin Measured by PRO-C6 as a Prognostic Biomarker for Liver-Related Events in Patients With Advanced Chronic Liver Disease.Liver international : official journal of the International Association for the Study of the Liver · 2026
    Article
  3. Observational
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
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  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. The Role ofCancers · 2025
    Review
  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

7 authors at 3 institutions in 2 countries.

Kim HenriksenDepartment of Cardiovascular Disease, Nordic Bioscience A/S, DK-2730 Herlev, Denmark.
Federica GenoveseDepartment of Cardiovascular Disease, Nordic Bioscience A/S, DK-2730 Herlev, Denmark.
Alexander Reese-PetersenDepartment of Cardiovascular Disease, Nordic Bioscience A/S, DK-2730 Herlev, Denmark.
Laurent P AudolyPrivebio Inc., Boston, MA 02445, USA.
Kai SunCenter for Metabolic and Degenerative Diseases, Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Morten A KarsdalDepartment of Cardiovascular Disease, Nordic Bioscience A/S, DK-2730 Herlev, Denmark.
Philipp E SchererTouchstone Diabetes Center, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.ORCID 0000-0003-0680-3392
Nordic Bioscience (Denmark) · DKThe University of Texas Health Science Center at Houston · USThe University of Texas Southwestern Medical Center · US

Funding

The role of AgRP/Auga-ALK pathway in FGF21's brain action on agingP01AG051459 · NIA · YALE UNIVERSITY · PI PHILIPP E SCHERER · 2016 to 2026
$25.7M
Adiponectin, A Protein Secreted From Adipose TissueR01DK055758 · NIDDK · YESHIVA UNIVERSITY · PI SCHERER, PHILIPP E · 2000 to 2024
$10.9M
Generation of Novel Genetic Tools to Study Cellular Heterogeneity in Adipose TissuesRC2DK118620 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI GUPTA, RANA K, SCHERER, PHILIPP E · 2019 to 2023
$7.0M
White Adipose Tissue Physiology, Mitochondrial Function and AdiponectinR01DK099110 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI PHILIPP E SCHERER · 2013 to 2026
$6.7M
Metabolic Benefits of Leptin ReductionR01DK127274 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI JOEL K. ELMQUIST, PHILIPP E SCHERER · 2021 to 2026
$5.1M
Physiological Role of Dedifferentiating Dermal Adipose TissueR01DK131537 · NIDDK · UT SOUTHWESTERN MEDICAL CENTER · PI SCHERER, PHILIPP E · 2022 to 2025
$2.1M
Dichotomous Effects of MT1-MMP on Adipose Tissue RemodelingR01DK109001 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SUN, KAI · 2017 to 2021
$2.0M
Discovering the new function of DRP1 on lipid metabolismR01DK129815 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SUN, KAI · 2022 to 2025
$1.5M
The unique role of Ces3 in PPAR-mediated thermogenesisR56DK124419 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI SUN, KAI · 2020 to 2020
$234k
NIA NIH HHS P01 AG051459NIDDK NIH HHS R01 DK055758NIDDK NIH HHS R01 DK099110NIDDK NIH HHS R01 DK109001NIDDK NIH HHS R01 DK127274NIDDK NIH HHS R01 DK129815NIDDK NIH HHS R01 DK131537NIDDK NIH HHS R56 DK124419NIDDK NIH HHS RC2 DK118620
6 · The paper itself

Abstract

Our overview covers several key areas related to recent results obtained for collagen type VI and endotrophin (ETP). (1) An introduction to the history of ETP, including how it was identified, how it is released, and its function and potential receptors. (2) An introduction to the collagen family, with a focus on what differentiates collagen type VI from an evolutionary standpoint. (3) An overview of collagen type VI, the 6 individual chains (COL6A1, A2, A3, A4, A5, and A6), their differences and similarities, as well as their expression profiles and function. (4) A detailed analysis of COL6A3, including the cleaved product endotrophin, and what separates it from the other 5 collagen 6 molecules, including its suggested function based on insights gained from knockout and gain of function mouse models. (5) The pathology of ETP. What leads to its presence and release and what are the consequences thereof? (6) Functional implications of circulating ETP. Here we review the data with the functional roles of ETP in mind. (7) We propose that ETP is a mediator for fibrotic (or fibroinflammatory) disorders. Based on what we know about ETP, we have to consider it as a target for the treatment of fibrotic (or fibroinflammatory) disorders. What segment(s) of the patient population would most dramatically respond to an ETP-targeted intervention? How can we find the population that would profit most from an intervention? We aim to present a broad overview over the ETP field at large, providing an assessment of where the future research efforts need to be placed to tap into the vast potential of ETP, both as a marker and as a target in different diseases.

Indexed as

BiomarkersCollagen Type VIPeptide FragmentsAnimalsFibrosisHumansInflammationBiomarkersCollagen Type VIendotrophinPeptide FragmentsColVIα3endotrophinextracellular matrixfibroinflammatory diseases

Identifiers

PMID38091968
PMCPMC11492497
OpenAlexW4389655169

What Socratic 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 Socratic graph.