Reactive gliosis and the multicellular response to CNS damage and disease

By J. Burda, M. Sofroniew. Neuron, 2014

1,318 citations recorded by the source corpus.

The central nervous system (CNS) is prone to heterogeneous insults of diverse etiologies that elicit multifaceted responses. Acute and focal injuries trigger wound repair with tissue replacement. Diffuse and chronic diseases provoke gradually escalating tissue changes. The responses to CNS insults involve complex interactions among cells of numerous lineages and functions, including CNS intrinsic neural cells, CNS intrinsic non-neural cells, and CNS extrinsic cells that enter from the circulation. The contributions of diverse non-neuronal cell types to outcome after acute injury, or to the progression of chronic disease, are of increasing interest as the push towards understanding and ameliorating CNS afflictions accelerates. In some cases considerable information is available, in others, comparatively little, as examined and reviewed here.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Neurology

View Paper: https://www.semanticscholar.org/paper/b560b45d85900f762105dde85925e8751a2c7e02

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. M. Pekny
2. M. Sofroniew
3. J. Burda
4. M. Pekna
5. E. Hol
6. Alexander M. Bernstein
7. J. Joyce
8. Alexei Verkhratsky

In Molecular Biology

1. M. Sofroniew
2. M. Pekny
3. M. Pekna
4. J. Burda
5. J. Joyce
6. Eric C. Holland
7. C. Steinhäuser
8. Alexei Verkhratsky

In Neurology

1. M. Pekny
2. M. Sofroniew
3. M. Pekna
4. J. Burda
5. E. Hol
6. Alexei Verkhratsky
7. Alexander M. Bernstein
8. Yilong Ren

Citations in the corpus

• Macrophage activation and its role in repair and pathology after spinal cord injury. (2015, background): “ECM and collagen formation after SCI follows a similar time course to that of skin and muscle wounds (Gurtner et al., 2008; Burda and Sofroniew, 2014; Gaudet and Popovich, 2014), however, components of the ECM drive protracted inflammation and impair wound closure (Gaudet and Popovich, 2014).”
• Physiology of Astroglia. (2018, neutral): “Finally, through mounting reactive response, astrocytes (together with microglia) represent the main defensive system of the CNS (we shall not discuss astrogliopathology in the present paper, instead recommending recent comprehensive reviews (257, 258, 1329, 1352, 1353, 1637, 1638, 1815, 1818).”
• Astrocytes: a central element in neurological diseases (2016, background): “Defensive function of astrocytes is manifested as reactive astrogliosis, a multicomponent and complex remodelling of astroglia triggered by lesions to the CNS [30, 169, 175, 210].”
• Astrocyte roles in traumatic brain injury (2015, background): “In response to focal tissue damage or inflammation, reactive astrocytes form scar borders that segregate damaged and inflamed tissue from adjacent potentially viable neural tissue (Sofroniew and Vinters, 2010; Burda and Sofroniew, 2014; Sofroniew, 2014b).”
• Spinal Cord Injury: Pathophysiology, Multimolecular Interactions, and Underlying Recovery Mechanisms (2020, background): “Sci. 2020, 21, x FOR PEER REVIEW 11 of 35 Astrocyte scar formation is driven by proliferation signals released by serum proteins and cells, such as thrombin, endothelin, FGF2, ATP, bone morphogenic proteins (BMPs), and sonic hedgehog (SHH) [41,43].”
• Astrocyte reactivity and reactive astrogliosis: costs and benefits. (2014, background): “The concept of reactive astrogliosis and its molecular and cellular definition is still incomplete, and we are only starting to understand its multifaceted functions in disease pathogenesis and in the process of recovery from CNS injuries (17, 34, 52, 146, 210, 221) (FIGURE 1).”
• Astrocyte reactivity: Subtypes, states and functions in CNS innate immunity (2020, background): “Proliferative, border-forming reactive astrocytes surround damaged tissue that contains leukocyte infiltration, stromal-cell proliferation and fibrosis after trauma, ischemia, infection, autoimmune inflammation, toxin accumulation, blood-brain barrier (BBB) leak or neurodegenerative disease (Key Fig”
• Glial fibrillary acidic protein (GFAP) and the astrocyte intermediate filament system in diseases of the central nervous system. (2015, background): “affects both the disease progression and the recovery process [20,21 ,22].”
• Spinal cord injury: molecular mechanisms and therapeutic interventions (2023, background): “In the distal area of the lesion, continuous with the astrocyte scar, the spare but reactive neural tissue contains neurons, astrocytes, oligodendrocytes, OPCs, and microglia.(172,175) The features of this compartment include reactive astrocytes and OPCs with a hypertrophic cell morphology, and this”
• The tumor microenvironment underlies acquired resistance to CSF1R inhibition in gliomas (2016, background): “During gliosis, activated macrophages play a central role in providing growth factors and signaling molecules to nearby astrocytes and neurons to form a reactive barrier that limits the extent of tissue damage in the brain (18, 20).”