Abstract
Cardiovascular pathologies are often induced by inflammation. The associated changes in the inflammatory response influence vascular endothelial biology; they complicate the extent of ischaemia and reperfusion injury, direct the migration of immune competent cells and activate platelets. The initiation and progression of inflammation is regulated by the classical paradigm through the system of cytokines and chemokines. Therapeutic approaches have previously used this knowledge to control the extent of cardiovascular changes with varying degrees of success. Neuronal guidance proteins (NGPs) have emerged in recent years and have been shown to be significantly involved in the control of tissue inflammation and the mechanisms of immune cell activation. Therefore, proteins of this class might be used in the future as targets to control the extent of inflammation in the cardiovascular system. In this review, we describe the role of NGPs during cardiovascular inflammation and highlight potential therapeutic options that could be explored in the future.
Highlights
Background and rationaleInflammation is an integral response of the human body that protects tissues challenged with sterile or nonsterile offenders [51]
Inhibition or activation of Neuronal guidance proteins (NGPs) pathways has been shown to effectively regulate the extent of organ damage and disease outcomes [21, 54, 72]. This narrative review summarizes the current state of the literature on NGPs and the inflammatory components of coronary artery disease and consecutive myocardial ischaemia and reperfusion injury
The essential role of neuronal guidance proteins in modulating inflammation during the course of coronary artery disease and myocardial ischaemia has been documented by a number of reports
Summary
Rap Ras-related protein 1 RBC Red blood cells RGM Repulsive guidance molecule Sema3A Semaphorin 3A Sema3E Semaphorin 3E Sema4C Semaphorin 4C Sema4D Semaphorin 4D Sema Semaphorin 7A shRNA Small hairpin ribonucleic acid siRNA Small interfering ribonucleic acid Smad Mothers against decapentaplegic homologue 3 Stat Signal transducers and activator of transcription 3 Syk Spleen tyrosine kinase TGF-β Transforming growth factor β TNFα Tumour necrosis factor α VCAM-1 Vascular cell adhesion molecule 1 VEGF (A/B) Vascular endothelial growth factor (A/B) VEGFR Vascular endothelial growth factor receptor VSMC Vascular smooth muscle cell
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