Adipose tissue depots and inflammation: effects on plasticity and resident mesenchymal stem cell function

Adipose tissue (AT) is a highly heterogeneous organ. Beside the heterogeneity associated to different tissue types (white, brown, and ‘brite’) and its location-related heterogeneity (subcutaneous, visceral, epicardial, and perivascular, etc.), AT composition, structure, and functionality are highly dependent on individual-associated factors.

As such, the pro-inflammatory state associated to the presence of obesity and other cardiovascular risk factors (CVRFs) directly affects AT metabolism. Furthermore, the adipose-derived stem cells (ASCs) that reside in the stromal vascular fraction of AT, besides being responsible for most of the plasticity attributed to AT, is an additional source of heterogeneity.

Thus, ASCs directly contribute to AT homeostasis, cell renewal, and spontaneous repair. These ASCs share many properties with the bone-marrow mesenchymal stem cells (i.e. potential to differentiate towards multiple tissue lineages, and angiogenic, antiapoptotic, and immunomodulatory properties).

Moreover, ASCs show clear advantages in terms of accessibility and quantity of available sample, their easy in vitro expansion, and the possibility of having an autologous source. All these properties point out towards a potential use of ASCs in regenerative medicine. However, the presence of obesity and other CVRFs induces a pro-inflammatory state that directly impacts ASCs proliferation and differentiation capacities affecting their regenerative abilities.

The focus of this review is to summarize how inflammation affects the different AT depots and the mechanisms by which these changes further enhance the obesity-associated metabolic disturbances.

Furthermore, we highlight the impact of obesity-induced inflammation on ASCs properties and how those effects impair their plasticity.

https://academic.oup.com/cardiovascres/article-abstract/doi/10.1093/cvr/cvx096/3819204/Adipose-tissue-depots-and-inflammation-effects-on?redirectedFrom=fulltext

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