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Angiogenesis modulates adipogenesis and obesity
Open accessAbstract
Substantial evidence shows that neoplastic and nonneoplastic tissue growth is dependent on angiogenesis. Neovascularization and adipogenesis are temporally and spatially coupled processes during prenatal life and they continue to reciprocally interact via paracrine signaling systems throughout adult life. Activated adipocytes produce multiple angiogenic factors including leptin, angiopoietins, HGF, GM-CSF, VEGF, FGF-2, and TGF-beta, which either alone or collectively stimulate neovascularization during fat mass expansion. Thus antiangiogenic agents provide a novel therapeutic option for prevention and treatment of human obesity and its related disorders.
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“The newly formed vascular network is crucial for adipogenesis and AT expansion (64,65).”
From Adipose tissue remodeling and obesity (2011) · cites this paper as [64]
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“Therefore, fetal and neonatal stages are the most effective stages to alter intramuscular adipocyte formation, followed by the weaning to 250 d of age, the so called marbling window (Corah and McCully, 2007).”
BackgroundA miR-327–FGF10–FGFR2-mediated autocrine signaling mechanism controls white fat browning
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The Effect of Processing Technique on Fat Graft Survival
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“lactation [4] and the expansion of fat mass during obesity [5] [6].”
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“Adipose tissue is highly vascularized, indicating that remodeling of the vascularization takes place during its hypertrophy (39, 41).”
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“To sustain vessel numbers, vascular integrity, and architectures, adipocytes, together with other cell types including inflammatory cells and mesenchymal cells, produce a variety of soluble and nonsoluble factors, cytokines, and adipokines to modulate vascular functions through a paracrine mechanism (7).”
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“Adipose tissue expansion is a dynamic process that involves adipocyte hypertrophy in combination with vascular re-modelling involving endothelial cells, macrophages and the extracellular matrix (13-16).”
BackgroundClinical and Genetic Correlates of Circulating Angiopoietin-2 and Soluble Tie-2 in the Community
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BackgroundMetabolic Rescue of Obese Adipose-Derived Stem Cells by Lin28/Let7 Pathway
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“Interestingly, the proportion of FAPs was greater in Brahman, while vascular cells were more abundant in Wagyu (Figure 1C), which may contribute to the lower adipogenic activity in Brahman muscle as vascularization supports adipogenesis.(7) Consistently, the capillary abundance was greater in Wagyu versus Brahman musc…”
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“Activated adipocytes produce multiple angiogenic factors including leptin, angiopoietins, hepatocyte growth factor (HGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) and transforming growth factor β (TGF-β), which either a…”
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Advances in an active and passive targeting to tumor and adipose tissues
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“DIO is involved in the up- and down-regulation of bio-macromolecules that facilitate the development of obesity, its-related metabolic syndrome and associated toxicities [23, 24].”
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Self-citationInhibition of the methionine aminopeptidase 2 enzyme for the treatment of obesity
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“Similar to cancer cells, brown adipose tissue (BAT) is highly vascularized tissue, and white adipose tissue (WAT) undergoes expansion and shrinkage throughout the life.(18) Owing to this nature, continuous remodeling of capillary networks, ie, dynamic angiogenesis, is required in both BAT and WAT.”
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White Adipose Tissue Dysfunction: Pathophysiology and Emergent Measurements
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“A healthy AT expansion is characterized by AT enlargement due more to adipocyte proliferation than to adipocyte hypertrophy [19,20], an increased angiogenic response that is proportional to adipose tissue enlargement [21], an adequate extracellular matrix (ECM) remodeling [22], and minimal inflammation.”
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“For instance, the level of VEGF production is higher in omental fat than in fat located at any other site in the body [18] and serum VEGF levels have been shown to correlate positively with visceral fat but not subcutaneous fat [5].”
Background
Metadata
- Authors
- Cao, Y.
- Affiliations
- Karolinska Institutet (SE)
- Corresponding author
- Cao, Yihai
- ORCID
- Cao, Yihai
- Venue
- Journal of Clinical Investigation
- Published
- 2007-09-04
- Volume
- 117
- Issue
- 9
- Pages
- 2362-2368
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1963348
- OpenAlex
- W2027442301
- Cited by
- 736
- References
- 120
- Citations by year
- 2026: 18 · 2025: 18 · 2024: 24 · 2023: 32 · 2022: 32 · 2021: 25 · 2020: 43 · 2019: 47 · 2018: 59 · 2017: 48 · 2016: 40 · 2015: 42 · 2014: 66 · 2013: 67 · 2012: 43
- FWCI
- 21.41
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Swedish Cancer Foundation
- European Commission
- Hjärt-Lungfonden
- Karolinska Institutet
- Vetenskapsrådet
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- angiogenesis, adipogenesis, obesity, neovascularization, adipocytes, angiogenic factors, leptin, vascular endothelial growth factor, angiopoietins, paracrine signaling, anti-angiogenic therapy
- MeSH terms
- Animals, Cell Communication, Humans, Neovascularization, Pathologic, Obesity, Adipocytes, Endothelial Cells, Angiogenesis Inducing Agents, Adipogenesis
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