| First Author | Fan Z | Year | 2024 |
| Journal | Cell Rep | Volume | 43 |
| Issue | 7 | Pages | 114395 |
| PubMed ID | 38941187 | Mgi Jnum | J:357395 |
| Mgi Id | MGI:7709027 | Doi | 10.1016/j.celrep.2024.114395 |
| Citation | Fan Z, et al. (2024) Macrophages preserve endothelial cell specialization in the adrenal gland to modulate aldosterone secretion and blood pressure. Cell Rep 43(7):114395 |
| abstractText | Macrophages play crucial roles in organ-specific functions and homeostasis. In the adrenal gland, macrophages closely associate with sinusoidal capillaries in the aldosterone-producing zona glomerulosa. We demonstrate that macrophages preserve capillary specialization and modulate aldosterone secretion. Using macrophage-specific deletion of VEGF-A, single-cell transcriptomics, and functional phenotyping, we found that the loss of VEGF-A depletes PLVAP(+) fenestrated endothelial cells in the zona glomerulosa, leading to increased basement membrane collagen IV deposition and subendothelial fibrosis. This results in increased aldosterone secretion, called "haptosecretagogue" signaling. Human aldosterone-producing adenomas also show capillary rarefaction and basement membrane thickening. Mice with myeloid cell-specific VEGF-A deletion exhibit elevated serum aldosterone, hypokalemia, and hypertension, mimicking primary aldosteronism. These findings underscore macrophage-to-endothelial cell signaling as essential for endothelial cell specialization, adrenal gland function, and blood pressure regulation, with broader implications for other endocrine organs. |
