Cited by 960Adipokines, Inflammation, and Metabolic DiseasesAdipose Tissue and MetabolismCardiovascular Disease and Adiposity

Fibrosis and adipose tissue dysfunction.

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Sun, Kai, Tordjman, Joan, Clément, Karine, Scherer, Philipp E.·2013·Cell Metabolism

Abstract

Fibrosis is increasingly appreciated as a major player in adipose tissue dysfunction. In rapidly expanding adipose tissue, pervasive hypoxia leads to an induction of HIF1α that in turn leads to a potent profibrotic transcriptional program. The pathophysiological impact of adipose tissue fibrosis is likely to play an equally important role on systemic metabolic alterations as fibrotic conditions play in the liver, heart, and kidney. Here, we discuss recent advances in our understanding of the genesis, modulation, and systemic impact of excessive extracellular matrix (ECM) accumulation in adipose tissue of both rodents and humans and the ensuing impact on metabolic dysfunction.

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Crossref · 10.1016/j.cmet.2013.06.016

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  • In dysfunctional AT, HIF-1α fails to promote angiogenesis, inducing dysregulated ECM remodeling, resulting in fibrosis that disrupts proper angiogenesis and further exacerbates hypoxia.

    “in dysfunctional AT, HIF-1α fails to promote angiogenesis, inducing instead dysregulated ECM remodeling, resulting in fibrosis that disrupts proper angiogenesis, further exacerbating hypoxia in AT”

    From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Sun et al., 2013

    In “The role of HIF1α” (page unavailable), the paper says HIF1α fails to induce an effective angiogenic response in adipose tissue and instead promotes ECM synthesis and fibrosis. “Relationship to angiogenesis” says excess ECM can impede capillary proliferation, but it does not establish the claimed final step—that fibrosis thereby further exacerbates hypoxia. It notes that a direct link between local hypoxia and fibrosis in human adipose tissue has not been established. (LLM, conf=0.86)

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Authors
Sun, K., Tordjman, J., Clément, K., & Scherer, P. E.
Affiliations
  • The University of Texas Southwestern Medical Center (US)
  • Inserm (FR)
Corresponding author
Scherer, Philipp E.
Venue
Cell Metabolism
Publisher
Elsevier BV
Published
2013-10
Volume
18
Issue
4
Pages
470-477
ISSN
1550-4131 (ISSN-L)
OpenAlex
W1994809630
Cited by
960
References
58
Citations by year
2026: 66 · 2025: 69 · 2024: 73 · 2023: 85 · 2022: 114 · 2021: 99 · 2020: 86 · 2019: 79 · 2018: 71 · 2017: 70 · 2016: 65 · 2015: 48 · 2014: 31 · 2013: 4
FWCI
5.84
Type
journal article
Language
en
Open access
Locations
  • Cell Metabolism (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK 55758, R01DK055758, P01DK088761, R01DK099110)
Topics
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Disease and Adiposity
Keywords
adipose tissue fibrosis, adipose tissue dysfunction, hypoxia, HIF-1α, extracellular matrix accumulation, metabolic dysfunction, obesity
MeSH terms
Adipose Tissue, Fibrosis, Humans, Insulin Resistance, Obesity, Cytokines, Hypoxia-Inducible Factor 1, alpha Subunit

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