Abstract
The failure of axonal regeneration after spinal cord injury (SCI) results in permanent loss of sensorimotor function. The persistent presence of scar tissue, mainly fibrotic scar and astrocytic scar, is a critical cause of axonal regeneration failure and is widely accepted as a treatment target for SCI. Astrocytic scar has been widely investigated, while fibrotic scar has received less attention. Here, we review recent advances in fibrotic scar formation and its crosstalk with other main cellular components in the injured core after SCI, as well as its cellular origin, function, and mechanism. This study is expected to provide an important basis and novel insights into fibrotic scar as a treatment target for SCI.
Highlights
Fibrosis, which is defined as fibroblasts excessively depositing extracellular matrix (ECM) mainly composed of collagen (COL), fibronectin (FN), and laminin (LN), is a common reaction to injury and inflammation in the central nervous system (CNS) and peripheral organs (Bataller and Brenner, 2005; Lee and Kalluri, 2010; Travers et al, 2016; Lederer and Martinez, 2018; Mack, 2018; Dorrier et al, 2021)
Glast– Rasless transgenic mice in which the proliferation of fibroblasts is inhibited to attenuate fibrotic scarring after Spinal cord injury (SCI) exhibit a reduction in astrogliosis and disruption of the contiguous boundary of astrocytic scar (Dias et al, 2018). These results suggest a crosstalk between the astrocytic scar and fibrotic scar to maintain the structural stability of each scar type after SCI
After using RNAi to inhibit the expression of EphB2, the formation of astrocytic scar and fibrotic scar is inhibited, promoting axonal regeneration and myelination (Wu et al, 2021). These results indicate that the crosstalk between fibroblasts and astrocytes mediated by Ephrin-B2 and EphB2 is a therapeutic target after SCI, but specific intracellular signaling pathways require further exploration
Summary
Fibrosis, which is defined as fibroblasts excessively depositing extracellular matrix (ECM) mainly composed of collagen (COL), fibronectin (FN), and laminin (LN), is a common reaction to injury and inflammation in the central nervous system (CNS) and peripheral organs (Bataller and Brenner, 2005; Lee and Kalluri, 2010; Travers et al, 2016; Lederer and Martinez, 2018; Mack, 2018; Dorrier et al, 2021). Fibroblasts gradually proliferate, migrate, and corral a large number of macrophages in the injured core, forming a fibrotic scar adjacent to the medial side of the astrocytic scar (Göritz et al, 2011; Soderblom et al, 2013; Zhu et al, 2015a).
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