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. 2024 Jan;19(1):6–13. doi: 10.18502/jthc.v19i1.15531

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Copyright© 2024 Tehran University of Medical Sciences. Published by Tehran University of Medical Sciences.

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International license (https://creativecommons.org/licenses/by-nc/4.0/). Noncommercial uses of the work are permitted, provided the original work is properly cited.

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Leukemia inhibitory factor (LIF) can induce cardiovascular disease (CVD) by binding to the LIF receptor. The attachment induces angiogenic pathways, inflammation, and coagulation. LIF can stimulate vascular endothelial (VE)-cadherin expression by activating the signal transducer and activator of transcription (STAT) pathway and inducing Ras homolog family member A (RhoA protein). It affects CVD. This factor can also be mediated if vascular endothelial growth factor (VEGF), B-cell lymphoma-extra large (Bcl-xL), Wnt family member 5A (WnT5a), manganese superoxide dismutase (Mn-SOD), monocyte chemoattractant protein-1 (MCP-1), interleukin-8 (IL-8), and angiopoietin activate the angiogenesis mechanism, inducing angiogenesis in the heart muscle. The LIF factor can also affect the system by the following proteins: tissue factor, urokinase-type plasminogen activator (UPA), and fibrinogen.