Why the study?
Pathological adipose tissue expansion during obesity leads to cellular, paracrine, mechanical, and metabolic alterations with local and systemic effects, including diabetes and cardiovascular disease.
Key points are not available for this paper at this time.
Design
Review
Answers are grounded in this paper and cite their sources.
Warrants mechanistic studies on adipocyte-endothelial signaling; leaves open clinical translation in obesity-related CVD.
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.
No takes yet. Share an insight, caveat, or question.
Johnston et al. (2023) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: