ABSTRACT
Endothelial dysfunction is considered as the main hallmark of Preeclampsia (PE). Despite the unknown pathogenesis of PE, different possible causes have been suggested in various studies. In this review, we first studied the Leukemia inhibitory factor (LIF) role in the related pathways to the PE pathogenesis, such as inflammation, endothelial dysfunction and hypertension. LIF can increase the expression of ICAM-1 and VCAM-1 via the JAK/STAT3 pathway, thereby inducing inflammatory responses and endothelial dysfunction. It can also be involved in the vascular vasoconstriction and hypertension by reducing the nitric oxide (NO) synthesis. Identifying the link between LIF and pathways associated with PE pathogenesis could be effective to achieve an effective PE treatment in the future.
Subject(s)
Leukemia Inhibitory Factor/physiology , Pre-Eclampsia/etiology , Signal Transduction/physiology , Female , Humans , Molecular Biology , Pre-Eclampsia/physiopathology , PregnancyABSTRACT
Aspirin-exacerbated respiratory disease (AERD) is characterized by immune cells dysfunction. This study aimed to investigate the molecular mechanisms involved in AERD pathogenesis. Relevant literatures were identified by a PubMed search (2005-2019) of english language papers using the terms "Aspirin-exacerbated respiratory disease", "Allergic inflammation", "molecular mechanism" and "mutation". According to the significant role of inflammation in AERD development, ILC-2 is known as the most important cell in disease progression. ILC-2 produces cytokines that induce allergic reactions and also cause lipid mediators production, which activates mast cells and basophils, ultimately. Finally, Monoclonal antibody and Aspirin desensitization in patients can be a useful treatment strategy for prevention and treatment.
