Biology of neurofibrosis with focus on multiple sclerosis

Brian M Lozinski; Samira Ghorbani; V Wee Yong

doi:10.3389/fimmu.2024.1370107

Biology of neurofibrosis with focus on multiple sclerosis

Front Immunol. 2024 Mar 26:15:1370107. doi: 10.3389/fimmu.2024.1370107. eCollection 2024.

Authors

Brian M Lozinski¹, Samira Ghorbani¹, V Wee Yong¹

Affiliation

¹ Hotchkiss Brain Institute and the Department of Clinical Neuroscience, University of Calgary, Calgary, AB, Canada.

Abstract

Tissue damage elicits a wound healing response of inflammation and remodeling aimed at restoring homeostasis. Dysregulation of wound healing leads to accumulation of effector cells and extracellular matrix (ECM) components, collectively termed fibrosis, which impairs organ functions. Fibrosis of the central nervous system, neurofibrosis, is a major contributor to the lack of neural regeneration and it involves fibroblasts, microglia/macrophages and astrocytes, and their deposited ECM. Neurofibrosis occurs commonly across neurological conditions. This review describes processes of wound healing and fibrosis in tissues in general, and in multiple sclerosis in particular, and considers approaches to ameliorate neurofibrosis to enhance neural recovery.

Keywords: CNS; ECM; MS; fibrosis; neurofibrosis; scarring.

Publication types

Review
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, Non-U.S. Gov't

MeSH terms

Biology
Central Nervous System
Fibrosis
Humans
Multiple Sclerosis*
Wound Healing

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. The authors’ research on neurofibrosis is supported by operating grants from the Canadian Institutes of Health Research (number 1049959), Multiple Sclerosis Canada (number 3527) and the USA Department of Defense MS Research program (contract number W81XWH2210468).