Fibrosis and Adipose Tissue Dysfunction
By K. Sun, J. Tordjman, Karine Clément, P. Scherer. Cell Metabolism, 2013
859 citations recorded by the source corpus.
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 pro-fibrotic 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.
Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Surgery
View Paper: https://www.semanticscholar.org/paper/b0c5595eba50865cd49f58ab40e6b99d4bf20c50
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Citations in the corpus
- Adipose tissue plasticity in health and disease (2022, background): “Obesity in mice and humans is generally associated with increased adipose-tissue fibrosis, especially in visceral depots, with higher levels of fibrosis correlating with more metabolic complications (Sun et al., 2013b).”
- Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans with Obesity. (2016, background): “It has been proposed that a pathological expansion of adipose tissue mass causes an increase in adipose tissue inflammation, manifested by alterations in adipose tissue immune cell populations and increased gene expression of pro-inflammatory cytokines and chemokines, which cause systemic inflammati”
- What We Talk About When We Talk About Fat (2014, neutral): “Current thinking holds that relaxation of the matrix allows healthy expansion of the fat pad; if the matrix is too rigid, then adipocytes become limited in their ability to store excess nutrients, and this leads to pathological features that include activation of stress-related pathways, inflammatio”