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. 2022 Jan 19;42:5. doi: 10.1186/s41232-021-00189-0

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© The Author(s) 2022

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — Role of semaphorins in the development of diabetic complications. Sema3A exaggerates diabetic retinopathy via the breakdown of retinal endothelial cell barrier function and recruitment of proangiogenic microglia. In the kidney, Sema3A disrupts the glomerular filtration barrier, contributing to the development of diabetic nephropathy. In contrast, Sema3A exerts osteoprotective effects, leading to the suppression of diabetic osteoporosis