Evidence map›Paper›PMID 37383542›Full record

ArticleLife metabolism2023

Extracellular matrix remodelling in obesity and metabolic disorders.

Vishal Musale, David H Wasserman, Li Kang

Open access · diamondAbstract read
In one paragraph

Article in Life metabolism, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
11.2field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
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  8. Muscle Ultrasound Echo Intensity Detects Insulin Resistance Before Changes in HbAJournal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine · 2026
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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.

Vishal MusaleDivision of Systems Medicine, School of Medicine, University of Dundee, Dundee, Scotland DD1 9SY, UK.
David H WassermanDepartment of Molecular Physiology and Biophysics, Mouse Metabolic Phenotyping Center, Vanderbilt University, Nashville, TN 37235, USA.
Li KangDivision of Systems Medicine, School of Medicine, University of Dundee, Dundee, Scotland DD1 9SY, UK.
University of Dundee · GBVanderbilt University · US

Funding

Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
INTEGRATED CONTROL OF MUSCLE GLUCOSE UPTAKE IN VIVOR01DK054902 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 1999 to 2020
$5.9M
Role of the Cell Adhesome in Obesity-related Liver DiseasesR01DK050277 · NIDDK · VANDERBILT UNIVERSITY · PI MCGUINNESS, OWEN P · 1995 to 2023
$4.8M
Exercise and Fuel MetabolismR37DK050277 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2008 to 2017
$4.2M
Vanderbilt Center for Metabolic Phenotyping in Live Models of Obesity and DiabetesU2CDK135073 · NIDDK · VANDERBILT UNIVERSITY · PI Julio E Ayala · 2023 to 2026
$3.8M
Integrated Control of Muscle Glucose Uptake in VivoR56DK054902 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2009 to 2009
$388k
British Heart Foundation PG/18/56/33935NIDDK NIH HHS R01 DK050277NIDDK NIH HHS R01 DK054902NIDDK NIH HHS R37 DK050277NIDDK NIH HHS R56 DK054902NIDDK NIH HHS U24 DK059637NIDDK NIH HHS U2C DK135073
6 · The paper itself

Abstract

Obesity causes extracellular matrix (ECM) remodelling which can develop into serious pathology and fibrosis, having metabolic effects in insulin-sensitive tissues. The ECM components may be increased in response to overnutrition. This review will focus on specific obesity-associated molecular and pathophysiological mechanisms of ECM remodelling and the impact of specific interactions on tissue metabolism. In obesity, complex network of signalling molecules such as cytokines and growth factors have been implicated in fibrosis. Increased ECM deposition contributes to the pathogenesis of insulin resistance at least in part through activation of cell surface integrin receptors and CD44 signalling cascades. These cell surface receptors transmit signals to the cell adhesome which orchestrates an intracellular response that adapts to the extracellular environment. Matrix proteins, glycoproteins, and polysaccharides interact through ligand-specific cell surface receptors that interact with the cytosolic adhesion proteins to elicit specific actions. Cell adhesion proteins may have catalytic activity or serve as scaffolds. The vast number of cell surface receptors and the complexity of the cell adhesome have made study of their roles challenging in health and disease. Further complicating the role of ECM-cell receptor interactions is the variation between cell types. This review will focus on recent insights gained from studies of two highly conserved, ubiquitously axes and how they contribute to insulin resistance and metabolic dysfunction in obesity. These are the collagen-integrin receptor-IPP (ILK-PINCH-Parvin) axis and the hyaluronan-CD44 interaction. We speculate that targeting ECM components or their receptor-mediated cell signalling may provide novel insights into the treatment of obesity-associated cardiometabolic complications.

Indexed as

extracellular matrixfibrosisinsulin resistancemetabolismobesity

Identifiers

PMID37383542
PMCPMC10299575
OpenAlexW4378470171

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.