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. 2025 Jan 13;14(1):2449027. doi: 10.1080/21623945.2024.2449027

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© 2025 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The terms on which this article has been published allow the posting of the Accepted Manuscript in a repository by the author(s) or with their consent.

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Angiotensin 1–7 reduces TNF-α secretion in a model of macrophage lipotoxicity. — Ang 1–7 reduces TNF-α secretion in a model of macrophage lipotoxicity. (a) TNF-α concentrations in the culture medium of LPS- and PA-treated RAW264.7 cells. CON, cells treated with only LPS and PA (control group); Ang 1–7, cells treated with LPS, PA, and Ang 1–7; Ang 1–7+A779, cells treated with LPS, PA, Ang 1–7, and A779. n = 14 for each group. Data are presented as means ± SE. **p < 0.01. (b) Schematic diagram showing the mechanism by which Ang 1–7 reduces inflammation in WAT in obesity. Macrophage-derived TNF-α not only impairs insulin signalling but also stimulates adipocytes to enhance more MCP-1 secretion in obesity. Interaction between adipocyte and macrophage forms a vicious cycle to augment inflammation. Ang 1–7 breaks this vicious cycle by acting on adipocytes and macrophages to reduce MCP-1 and TNF-α secretion, respectively.