Monocyte Transmodulation: The Next Novel Therapeutic Approach in Overcoming Ischemic Stroke?

Joohyun Park,Jong Youl Kim,Jong Eun Lee,Ji Young Chang

doi:10.3389/fneur.2020.578003

Abstract

The immune response following neuroinflammation is a vital element of ischemic stroke pathophysiology. After the onset of ischemic stroke, a specialized vasculature system that effectively protects central nervous system tissues from the invasion of blood cells and other macromolecules is broken down within minutes, thereby triggering the inflammation cascade, including the infiltration of peripheral blood leukocytes. In this series of processes, blood-derived monocytes have a significant effect on the outcome of ischemic stroke through neuroinflammatory responses. As neuroinflammation is a necessary and pivotal component of the reparative process after ischemic stroke, understanding the role of infiltrating monocytes in the modulation of inflammatory responses may offer a great opportunity to explore new therapies for ischemic stroke. In this review, we discuss and highlight the function and involvement of monocytes in the brain after ischemic injury, as well as their impact on tissue damage and repair.

Highlights

Stroke is the third leading cause of death globally, and ∼80% of all strokes are ischemic strokes, which occur when brain cells die of reduced blood supply to various parts of the brain [1,2,3]
These results indicate that CXC motif chemokine receptor 4 (CXCR4) distinguishing hematopoietic stem cells (HSCs)-derived monocytes from microglia is a crucial factor in sustaining the beneficial role of monocytes through an innate immune system against neuroinflammation following ischemic stroke [116]
The evidence discussed here suggests that the application of transcriptomics and epigenomics targeting monocyte/macrophage plays a crucial role in the regulation of neuroinflammation following ischemic stroke

Summary

Introduction

Stroke is the third leading cause of death globally, and ∼80% of all strokes are ischemic strokes, which occur when brain cells die of reduced blood supply to various parts of the brain [1,2,3]. The regulation of transforming growth factor βactivated kinase 1 (TAK1), which is involved in both innate and adaptive immune responses and has conflicting inflammatory effects depending on the cell type, plays a key role in monocyte infiltration into the injury site following ischemic stroke.

Results

Conclusion