Adipose Tissue Paracrine-, Autocrine-, and Matrix-Dependent Signaling during the Development and Progression of Obesity

Obesity is an ever-increasing phenomenon, with 42% of Americans being considered obese (BMI >= 30) and 9.2% being considered morbidly obese (BMI >= 40) as of 2016. With obesity being characterized by an abundance of adipose tissue expansion, abnormal tissue remodeling is a typical consequence. Importantly, this pathological tissue expansion is associated with many alterations in the cellular populations and phenotypes within the tissue, lending to cellular, paracrine, mechanical, and metabolic alterations that have local and systemic effects, including diabetes and cardiovascular disease. In particular, vascular dynamics shift during the progression of obesity, providing signaling cues that drive metabolic dysfunction. In this review, paracrine-, autocrine-, and matrix-dependent signaling between adipocytes and endothelial cells is discussed in the context of the development and progression of obesity and its consequential diseases, including adipose fibrosis, diabetes, and cardiovascular disease.

Automated summary

Obesity is a growing problem, with a significant number of Americans being obese or morbidly obese. Tissue remodeling and changes in cellular populations and phenotypes occur as a result of pathological tissue expansion. This leads to local and systemic effects, including diabetes and cardiovascular disease. Vascular dynamics play a role in metabolic dysfunction during obesity progression. This review focuses on paracrine, autocrine, and matrix-dependent signaling between adipocytes and endothelial cells in the development and progression of obesity and related diseases.