Angiogenesis in adipose tissue and obesity

Corvera, Silvia; Solivan-Rivera, Javier; Loureiro, Zinger Yang

doi:10.1007/s10456-022-09848-3

Cited by 62 publications

(32 citation statements)

References 157 publications

(224 reference statements)

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“…6 Two mechanisms of adipose tissue expansion. During adipose tissue expansion, cells of the vasculature, adipose progenitor cells, and adipocytes encounter multiple signaling interactions, involving hypoxia, insulin/insulin-like growth factors and vascular guidance cues (apelin/apelin receptor, VEGF, angiopoietins) [ 212 , 387 ]. A An increase in fat tissue under physiological conditions results from hyperplastic expansion where small adipocytes are generated from multipotent progenitor cells.…”

Section: Angiogenesis and Anti-angiogenesis In Diseasesmentioning

confidence: 99%

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Pathological angiogenesis: mechanisms and therapeutic strategies

Dudley

2023

Angiogenesis

153

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In multicellular organisms, angiogenesis, the formation of new blood vessels from pre-existing ones, is an essential process for growth and development. Different mechanisms such as vasculogenesis, sprouting, intussusceptive, and coalescent angiogenesis, as well as vessel co-option, vasculogenic mimicry and lymphangiogenesis, underlie the formation of new vasculature. In many pathological conditions, such as cancer, atherosclerosis, arthritis, psoriasis, endometriosis, obesity and SARS-CoV-2(COVID-19), developmental angiogenic processes are recapitulated, but are often done so without the normal feedback mechanisms that regulate the ordinary spatial and temporal patterns of blood vessel formation. Thus, pathological angiogenesis presents new challenges yet new opportunities for the design of vascular-directed therapies. Here, we provide an overview of recent insights into blood vessel development and highlight novel therapeutic strategies that promote or inhibit the process of angiogenesis to stabilize, reverse, or even halt disease progression. In our review, we will also explore several additional aspects (the angiogenic switch, hypoxia, angiocrine signals, endothelial plasticity, vessel normalization, and endothelial cell anergy) that operate in parallel to canonical angiogenesis mechanisms and speculate how these processes may also be targeted with anti-angiogenic or vascular-directed therapies.

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Section: Angiogenesis and Anti-angiogenesis In Diseasesmentioning

confidence: 99%

“…The latter mechanism is strongly associated with metabolic disease risk. Figure adapted from Corvera et al, 2021 [ 212 ]. Figure is created with BioRender.com and is available on request …”

Section: Angiogenesis and Anti-angiogenesis In Diseasesmentioning

confidence: 99%

Pathological angiogenesis: mechanisms and therapeutic strategies

Dudley

2023

Angiogenesis

153

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“…Interestingly, AT expansion in the femoral area is mainly through hyperplasia in adult men and women after 8 weeks in response to overfeeding [ 12 , 41 , 42 ]. A healthy expansion of AT requires precise coordination between adipocyte hypertrophy/hyperplasia, with adequate vascularization and remodeling of ECM [ 43 , 44 ]. In this sense, when the vasculature does not supply enough irrigation to a zone containing hypertrophic adipocytes, the latter could be exposed to hypoxia.…”

Section: Adipose Tissue Dysfunctionmentioning

confidence: 99%

White Adipose Tissue Dysfunction: Pathophysiology and Emergent Measurements

et al. 2023

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White adipose tissue (AT) dysfunction plays an important role in the development of cardiometabolic alterations associated with obesity. AT dysfunction is characterized by the loss of the expansion capacity of the AT, an increment in adipocyte hypertrophy, and changes in the secretion profile of adipose cells, associated with accumulation of macrophages and inflammation. Since not all people with an excess of adiposity develop comorbidities, it is necessary to find simple tools that can evidence AT dysfunction and allow the detection of those people with the potential to develop metabolic alterations. This review focuses on the current pathophysiological mechanisms of white AT dysfunction and emerging measurements to assess its functionality.

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“…Impairments in angiogenic capacity also occur in obese VAT. Inhibition of angiogenesis leads to rarefaction of capillaries, impaired proliferation of multipotent progenitor cells, and adipocyte hypertrophy ( 110 ). These changes in the environment surrounding T cells may affect the intracellular metabolic system and induce T-cell exhaustion.…”

Section: Homeostatic and Pathogenic Role Of Cd4 T Cells In Vatmentioning

confidence: 99%

Drastic transformation of visceral adipose tissue and peripheral CD4 T cells in obesity

Shirakawa

Sano

2023

Front. Immunol.

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Obesity has a pronounced effect on the immune response in systemic organs that results in not only insulin resistance but also altered immune responses to infectious diseases and malignant tumors. Obesity-associated microenvironmental changes alter transcriptional expression and metabolism in T cells, leading to alterations in T-cell differentiation, proliferation, function, and survival. Adipokines, cytokines, and lipids derived from obese visceral adipose tissue (VAT) may also contribute to the systemic T-cell phenotype, resulting in obesity-specific pathogenesis. VAT T cells, which have multiple roles in regulating homeostasis and energy utilization and defending against pathogens, are most susceptible to obesity. In particular, many studies have shown that CD4 T cells are deeply involved in the homeostasis of VAT endocrine and metabolic functions and in obesity-related chronic inflammation. In obesity, macrophages and adipocytes in VAT function as antigen-presenting cells and contribute to the obesity-specific CD4 T-cell response by inducing CD4 T-cell proliferation and differentiation into inflammatory effectors via interactions between major histocompatibility complex class II and T-cell receptors. When obesity persists, prolonged stimulation by leptin and circulating free fatty acids, repetitive antigen stimulation, activating stress responses, and hypoxia induce exhaustion of CD4 T cells in VAT. T-cell exhaustion is characterized by restricted effector function, persistent expression of inhibitory receptors, and a transcriptional state distinct from functional effector and memory T cells. Moreover, obesity causes thymic regression, which may result in homeostatic proliferation of obesity-specific T-cell subsets due to changes in T-cell metabolism and gene expression in VAT. In addition to causing T-cell exhaustion, obesity also accelerates cellular senescence of CD4 T cells. Senescent CD4 T cells secrete osteopontin, which causes further VAT inflammation. The obesity-associated transformation of CD4 T cells remains a negative legacy even after weight loss, causing treatment resistance of obesity-related conditions. This review discusses the marked transformation of CD4 T cells in VAT and systemic organs as a consequence of obesity-related microenvironmental changes.

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Angiogenesis in adipose tissue and obesity

Cited by 62 publications

References 157 publications

Pathological angiogenesis: mechanisms and therapeutic strategies

Pathological angiogenesis: mechanisms and therapeutic strategies

White Adipose Tissue Dysfunction: Pathophysiology and Emergent Measurements

Drastic transformation of visceral adipose tissue and peripheral CD4 T cells in obesity

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