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. 2022 Jun 4;7:177. doi: 10.1038/s41392-022-01038-3

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — The regulated signaling pathways of PTP1B in inflammatory diseases. The role of PTP1B in insulin signaling, leptin signaling, and LPS-TLR-mediated inflammatory signaling in diabetes, obesity, and other inflammatory diseases. PTP1B inhibits the phosphorylation of the insulin receptor and insulin receptor substrate and their downstream PI3K/AKT/GLUT4 signaling, thereby preventing the translocation of GLUT4 to the membrane to transport glucose. PTP1B also inhibits JAK2 phosphorylation and attenuates the leptin JAK2/STAT signaling pathway to affect metabolic energy homeostasis. The CREB/KMT5A complex regulates PTP1B to modulate high glucose-induced endothelial inflammatory factor levels in diabetic nephropathy. PTP1B also acts as a negative regulator of TLR signaling via the suppression of both MyD88- and TRIF-dependent production of proinflammatory cytokines in macrophages stimulated by LPS