Evidence map›Paper›PMID 31988105›Full record

ArticleMolecular and cellular biology2020

Critical Role of Matrix Metalloproteinase 14 in Adipose Tissue Remodeling during Obesity.

Xin Li, Yueshui Zhao, Chuan Chen, Li Yang, Hyun-Ho Lee, Zening Wang, Ningyan Zhang, Mikhail G Kolonin, Zhiqiang An, Xin Ge and 2 more

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
4.6field-weighted citation impact, top 3% 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

61 citing papers in PubMed, 92 citations in OpenAlex.

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  18. Hypoxia signaling in the adipose tissue.Journal of molecular cell biology · 2025
    Review
  19. Is the endotoxin-complement cascade the major driver in lipedema?Trends in endocrinology and metabolism: TEM · 2024
    Review
  20. Article

1 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

12 authors at 3 institutions in 1 country.

Xin LiCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Yueshui ZhaoCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Chuan ChenDepartment of Chemical and Environmental Engineering, University of California, Riverside, California, USA.
Li YangCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Hyun-Ho LeeCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Zening WangDepartment of Chemical and Environmental Engineering, University of California, Riverside, California, USA.
Ningyan ZhangTexas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Mikhail G KoloninCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Zhiqiang AnTexas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA.
Xin GeDepartment of Chemical and Environmental Engineering, University of California, Riverside, California, USA.
Philipp E SchererTouchstone Diabetes Center, UT Southwestern Medical Center at Dallas, Dallas, Texas, USA.ORCID 0000-0003-0680-3392
Kai SunCenter for Metabolic and Degenerative Diseases, The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas Health Science Center at Houston, Houston, Texas, USA kai.sun@uth.tmc.edu.ORCID 0000-0002-4778-4549
Brown Foundation · USUniversity of California, Riverside · USSouthwestern Medical Center · US

Funding

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
Structure-based design of camel-like human selective mAbs against MMPs in diseaseR01GM115672 · NIGMS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI GE, XIN · 2016 to 2020
$1.5M
NIDDK NIH HHS R01 DK109001NIGMS NIH HHS R01 GM115672
6 · The paper itself

Abstract

Fibrosis is recognized as the major pathological change in adipose tissue during the development of obesity. However, the detailed mechanisms governing the interactions between the fibrotic components and their modifiers remain largely unclear. Here, we reported that matrix metalloproteinase 14 (MMP14), a key pericellular collagenase, is dramatically upregulated in obese adipose tissue. We generated a doxycycline-inducible adipose tissue-specific MMP14 overexpression model to study its regulatory function. We found that overexpression of MMP14 in the established obese adipose tissue leads to enlarged adipocytes and increased body weights in transgenic mice. Furthermore, the mice exhibited decreased energy expenditure, impaired lipid metabolism, and insulin resistance. Mechanistically, we found that MMP14 digests collagen 6α3 to produce endotrophin, a potent costimulator of fibrosis and inflammation. Unexpectedly, when overexpressing MMP14 in the early-stage obese adipose tissue, the transgenic mice showed a healthier metabolic profile, including ameliorated fibrosis and inflammation, as well as improved lipid and glucose metabolism. This unique metabolic phenotype is likely due to digestion/modification of the dense adipose tissue extracellular matrix by MMP14, thereby releasing the mechanical stress to allow for its healthy expansion. Understanding these dichotomous impacts of MMP14 provides novel insights into strategies to treat obesity-related metabolic disorders.

Indexed as

AdipocytesAdipose TissueAdiposityAnimalsCell LineEnergy MetabolismFemaleFibrosisHEK293 CellsHumansInflammationInsulinInsulin ResistanceMaleMatrix Metalloproteinase 14MiceInsulinMatrix Metalloproteinase 14MMP14 protein, humanMmp14 protein, mouseadipose tissuecollagen 6ECMendotrophinfibrosisHIF1inflammationlipid metabolismMMP14obesity

Identifiers

PMID31988105
PMCPMC7108820
OpenAlexW3003690690

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.