Breakdown of adipocyte-endothelial communication as a driver of adipose tissue dysfunction in obesity
Year: 2026
Type: review
Abstract: Obesity is associated with chronic low-grade inflammation, which is considered a critical factor underlying insulin resistance (IR), a major risk factor for the development of type 2 diabetes (T2D) and its detrimental sequelae including cardiovascular diseases (CVD). White adipose tissues (WAT), the intra-abdominal AT in particular, are key sites mediating the emergence of systemic low-grade inflammation. In obese adipose tissue the hypertrophy (expanded size) of adipocytes, coinciding with defective adipogenesis, results in a pathologic state of the adipose tissue characterized by reduced blood flow, pro-inflammatory activation, infiltration of inflammatory cells, and fibrosis. Healthy AT is highly vascularized and each adipocyte is in direct contact with at least one capillary. To maintain normal adipose tissue function, communication of the adipocytes with the endothelial cells (EC) is essential, and obesity involves the dysfunction of both adipocytes and EC. The defects in communication of these two cell types in obese AT involve a multitude of mechanisms and mediators: defective nitric oxide (NO), insulin and angiocrine regulation in endothelia, altered adipokine secretion by adipocytes, dysregulation of extracellular vesicles produced by both cell types, as well as altered lymphatic vessel function, endothelial-to-mesenchymal transition, and vascular remodeling. In this review we provide an overview of the current knowledge on the impacts of obesity on the communication between WAT adipocytes and endothelial cells, and how defects in this intercellular cross-talk may contribute to the pathologic sequelae of obesity.
Source: Frontiers in Endocrinology
Institutions: Minerva Foundation, University of Helsinki
Language: English
Subfield: Endocrinology, Diabetes and Metabolism
Field: Medicine
Domain: Health Sciences
Open Access status: gold
Estimated APC paid: $3,801
OpenAlex ID: W7221552443