4.7 Review

Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies

Journal

Publisher

MDPI
DOI: 10.3390/ijms23094995

Keywords

astrocytes; senescence; reactive astrogliosis; neurodegenerative diseases; SASP; astrocyte-targeted therapy; in vitro models

Funding

  1. Ministry of Education, Science and Technological Development, Republic of Serbia [451-03-68/2022-14/200042]
  2. Serbian Academy of Sciences and Arts [01-2021]

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This review summarizes the latest research on astrocyte reactivation and senescence, and compares their similarities and differences in terms of morphology, function, and molecular aspects. The article specifically focuses on the role of these cellular changes in neurodegenerative diseases, and discusses the potential of astrocytes as therapeutic targets.
Astrocytes, as the most abundant glial cells in the central nervous system, are tightly integrated into neural networks and participate in numerous aspects of brain physiology and pathology. They are the main homeostatic cells in the central nervous system, and the loss of astrocyte physiological functions and/or gain of pro-inflammatory functions, due to their reactivation or cellular senescence, can have profound impacts on the surrounding microenvironment with pathological outcomes. Although the importance of astrocytes is generally recognized, and both senescence and reactive astrogliosis have been extensively reviewed independently, there are only a few comparative overviews of these complex processes. In this review, we summarize the latest data regarding astrocyte reactivation and senescence, and outline similarities and differences between these phenotypes from morphological, functional, and molecular points of view. A special focus has been given to neurodegenerative diseases, where these phenotypic alternations of astrocytes are significantly implicated. We also summarize current perspectives regarding new advances in model systems based on astrocytes as well as data pointing to these glial cells as potential therapeutic targets.

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