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Nat. Rev. Nephrol. doi: /nrneph

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Presentation on theme: "Nat. Rev. Nephrol. doi: /nrneph"— Presentation transcript:

1 Nat. Rev. Nephrol. doi:10.1038/nrneph.2016.75
Figure 3 Potential role of adipokines in the development of obesity-related glomerulopathy Figure 3 | Potential role of adipokines in the development of obesity-related glomerulopathy. In obesity, satiated fat cells facilitate adipose tissue expansion by secreting angiogenic and inflammatory adipokines such as angiopoietins, vascular endothelial growth factor (VEGF), and cathepsins. These adipokines promote stromal rearrangements, neovascularization and the formation of novel adipocytes from pericytes of the microvasculature. Angiogenesis and adipogenesis are intricately linked, and disturbed angiogenesis has been associated with diminished adipose tissue expandability. Systemically circulating adipokines might reach the kidney and have local effects on mesangial cells, podocytes, and tubular cells, promoting maladaptive responses to glomerular hyperfiltration and albuminuria. Ang II, angiotensin II, HIF-1, hypoxia-inducible factor-1; MCP-1, monocyte chemoattractant protein-1 (also known as C-C motif chemokine 2); MMP, matrix metalloproteinase; NEFA, non-esterified fatty acid; TGF-β, transforming growth factor β. D’Agati, V. D. et al. (2016) Obesity-related glomerulopathy: clinical and pathologic characteristics and pathogenesis Nat. Rev. Nephrol. doi: /nrneph

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