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Deciphering the cellular interplays underlying obesity-induced adipose tissue fibrosis
Geneviève Marcelin, … , Adaliene V.M. Ferreira, Karine Clément
Geneviève Marcelin, … , Adaliene V.M. Ferreira, Karine Clément
Published September 9, 2019
Citation Information: J Clin Invest. 2019;129(10):4032-4040. https://doi.org/10.1172/JCI129192.
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Review Series

Deciphering the cellular interplays underlying obesity-induced adipose tissue fibrosis

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Abstract

Obesity originates from an imbalance between caloric intake and energy expenditure that promotes adipose tissue expansion, which is necessary to buffer nutrient excess. Patients with higher visceral fat mass are at a higher risk of developing severe complications such as type 2 diabetes and cardiovascular and liver diseases. However, increased fat mass does not fully explain obesity’s propensity to promote metabolic diseases. With chronic obesity, adipose tissue undergoes major remodeling, which can ultimately result in unresolved chronic inflammation leading to fibrosis accumulation. These features drive local tissue damage and initiate and/or maintain multiorgan dysfunction. Here, we review the current understanding of adipose tissue remodeling with a focus on obesity-induced adipose tissue fibrosis and its relevance to clinical manifestations.

Authors

Geneviève Marcelin, Ana Letícia M. Silveira, Laís Bhering Martins, Adaliene V.M. Ferreira, Karine Clément

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Figure 3

Adipose tissue fibrosis in obese subjects.

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Adipose tissue fibrosis in obese subjects.
With chronic obesity, WAT dep...
With chronic obesity, WAT depots undergo continual remodeling, becoming pathological. Combined with unadapted vascularization promoting hypoxia and unresolved inflammation, alteration of the equilibrium between the myofibroblast and the adipogenic fate of adipose progenitors is important in the unhealthy growth of adipose tissue. Various signals and transcription factors were found to be important in controlling the fate of progenitors.
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