Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaper › Review › Research › peer-review
Final published version
Obesity is a worldwide health problem, and as its prevalence increases, so does the burden of obesity-associated co-morbidities like type 2 diabetes or cardiovascular diseases (CVDs). Adipose tissue (AT) is an endocrine organ embedded in a dense vascular network. AT regulates the production of hormones, angiogenic factors, and cytokines. During the development of obesity, AT expands through the increase in fat cell size (hypertrophy) and/or fat cell number (hyperplasia). The plasticity and expansion of AT is related to its angiogenic capacities. Angiogenesis is a tightly orchestrated process, which involves endothelial cell (EC) proliferation, migration, invasion, and new tube formation. The expansion of AT is accelerated by hypoxia, inflammation, and structural remodeling of blood vessels. The paracrine signaling regulates the functional link between ECs and adipocytes. Adipocytes can secrete both pro-angiogenic molecules, e.g., tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), or vascular endothelial growth factor (VEGF), and anti-angiogenic factors, e.g., serpins. If the pro-angiogenic molecules dominate, the angiogenesis is dysregulated and the endothelium becomes dysfunctional. However, if anti-angiogenic molecules are overexpressed relative to the angiogenic regulators, the angiogenesis is repressed, and AT becomes hypoxic. Furthermore, in the presence of chronic nutritional excess, endothelium loses its primary function and contributes to the inflammation and fibrosis of AT, which increases the risk for CVDs. This review discusses the current understanding of ECs function in AT, the cross-talk between adipose and ECs, and how obesity can lead to its dysfunction. Understanding the interplay of angiogenesis with AT can be an approach to therapy obesity and obesity-related diseases such as CVDs.
Original language | English |
---|---|
Article number | 624903 |
Journal | Frontiers in Physiology |
Volume | 11 |
Number of pages | 9 |
ISSN | 1664-042X |
DOIs | |
Publication status | Published - Feb 2021 |
Funding Information:
We apologize for not being able to cite the work of all other studies related to this topic because of space restrictions. The figures were created with BioRender.com. Funding. JK is supported by the Lundbeck Fonden R307-2018-3667, by AIAS-CO-FUNDII:GA: MSCA: 754513 and Steno Diabetes Center Aarhus.
Publisher Copyright:
© Copyright © 2021 Herold and Kalucka.
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
See relations at Aarhus University Citationformats
ID: 217983716