Review
Version 1
Preserved in Portico This version is not peer-reviewed
TGF-β as a Key Modulator of Astrocyte Reactivity
Version 1
: Received: 18 April 2022 / Approved: 20 April 2022 / Online: 20 April 2022 (09:06:47 CEST)
A peer-reviewed article of this Preprint also exists.
Luo, J. TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications. Biomedicines 2022, 10, 1206. Luo, J. TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications. Biomedicines 2022, 10, 1206.
Abstract
Astrocytes are essential for normal brain development and functioning. They respond to brain injury and disease through a process referred to as reactive astrogliosis, where the reactivity is highly heterogenous and context dependent. Reactive astrocytes are active contributors to brain pathology and can exert beneficial, detrimental, or mixed effects following brain insults. Transforming growth factor-β (TGF-β) has been identified as one of the key factors regulating astrocyte reactivity. Genetic and pharmacological manipulation of TGF-β signaling pathway in animal models of CNS injury and disease alters pathological and functional outcomes. This review aims to provide recent understanding regarding astrocyte reactivity and TGF-β signaling in brain injury, aging, and neurodegeneration. Further, it explores how TGF-β signaling modulates astrocyte reactivity and function.
Keywords
astrocytes; reactive astrogliosis; TGF-β; traumatic brain injury; stroke; aging; Alzheimer’s disease; Parkinson’s disease; amyotrophic lateral sclerosis; multiple sclerosis; epilepsy
Subject
LIFE SCIENCES, Other
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Comments (0)
We encourage comments and feedback from a broad range of readers. See criteria for comments and our Diversity statement.
Leave a public commentSend a private comment to the author(s)