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TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications

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 an...

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Detalles Bibliográficos
Autor principal: Luo, Jian
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138510/
https://www.ncbi.nlm.nih.gov/pubmed/35625943
http://dx.doi.org/10.3390/biomedicines10051206
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author Luo, Jian
author_facet Luo, Jian
author_sort Luo, Jian
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description 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. The genetic and pharmacological manipulation of the TGF-β signaling pathway in animal models of central nervous system (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 in the context of CNS disease and injury.
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spelling pubmed-91385102022-05-28 TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications Luo, Jian Biomedicines Review 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. The genetic and pharmacological manipulation of the TGF-β signaling pathway in animal models of central nervous system (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 in the context of CNS disease and injury. MDPI 2022-05-23 /pmc/articles/PMC9138510/ /pubmed/35625943 http://dx.doi.org/10.3390/biomedicines10051206 Text en © 2022 by the author. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Luo, Jian
TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title_full TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title_fullStr TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title_full_unstemmed TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title_short TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications
title_sort tgf-β as a key modulator of astrocyte reactivity: disease relevance and therapeutic implications
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9138510/
https://www.ncbi.nlm.nih.gov/pubmed/35625943
http://dx.doi.org/10.3390/biomedicines10051206
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