Adipose Tissue in the Cardiovascular Homeostasis and Disease

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Background

Adipose tissue is the largest endocrine organ in the body, being composed predominantly of adipocytes (80%) and a diversity of other cells including fibroblasts, vascular endothelial cells and immune cells such as macrophages and T-cells. Further, adipose tissue is broadly dispersed within the bodily system and can be distributed as subcutaneous fat beneath the skin, visceral fat surrounding the blood vessels, heart, kidneys, and nerve tissue, as well as in the abdominal cavity and additionally stored intra-organ, as one would see with intramuscular fat or hepatic steatosis.

Under healthy conditions, adipose tissue is recognized as a key controller of cardiovascular homeostasis. However, changes in expansion and/or quality of adipose tissue, such as in obesity or lipodystrophy, cause the adipose tissue to become dysregulated and consequently change towards a villainous phenotype capable of secreting an abnormal number of bioactive products called adipokines, such as leptin, adiponectin, resistin and visfatin.

For example, weight gain in obesity leads an excess of fat which exacerbates the production of many adipokines, whereas, in a completely different scenario, lipodystrophy is characterized by a severe reduction in adipokines production via a drastic reduction in adipose tissue amount. However, obesity and lipodystrophy present several common disturbs such as diabetes and cardiovascular risk possibly due adipokines resistance and lack of adipokines production respectively.

Active receptors for adipokines are broadly expressed in mammalian cells, including vascular smooth cells, endothelial cells and immune cells, all of which can significantly contribute to cardiovascular health or disease. It is well accepted that adipose tissue plays a significant role in controlling the physiological function of the cardiovascular system. Further, evidence clearly supports the idea that perturbation of the adipose tissue, either through changes in quantity, quality, or malfunction can radically interfere with the function of an organism. Taken together, it is of vital importance that further research elucidates the mechanisms by which adipose tissue and its signaling cascades effect cardiovascular function and how derangement of such mechanisms ultimately drive cardiovascular dysfunction in disease states. Adipokines treatment or changes in the adipokines sensitivity in target organ might be promisor avenues to solve cardiovascular disease associated with changes in adiposity and adipokines production/bioavailability.

Therefore, the major goal of this call is to expand our understanding on the crosstalk between adipose tissue and cardiovascular system or any related area, and discuss new possibilities in improving of the adipokines sensitivity in different targets in order to minimize the cardiovascular risk. We invite scientists to spread and share their novel and innovative ideas, findings and discoveries on adipose tissue-derived products and cardiovascular system in physiological and pathophysiological conditions. This Research Topic welcomes in vitro, ex vivo and in vivo studies investigating how adipose tissue contributes to the cardiovascular function or dysfunction. We expect submissions of different types such as Original Research articles, Reviews, Mini-Reviews, Case Reports and Brief Research Reports focusing on, but not limited to, the following topics:

• Crosstalk between adipose tissue and cardiovascular system in physiological condition;
• Direct contribution of adipose tissue on cardiovascular disease development associated with different diseases, such as obesity, lipodystrophy, diabetes and hypertension;
• Adipokines effects on endothelial, smooth muscle, renal and immune cells;
• Adipose tissue inflammation and adipokines production;
• Possible pharmacological and/or genetic interventions in the adipose tissue and target organ

Keywords: Cardiovascular, adipose tissue, smooth muscle, endothelium and endocrinology

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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