Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?

Reich, Arno; Spering, Christopher; Schulz, Jörg B.

doi:10.1016/j.tins.2008.06.007

Cited by 46Cell death mechanisms and regulationNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?

Reich, Arno, Spering, Christopher, Schulz, Jörg B.·2008·Trends in Neurosciences

DOI 10.1016/j.tins.2008.06.007

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Abstract

For over a decade, neuroscientific research has focused on processes of apoptosis and its contribution to the pathophysiology of neurological diseases. In the central nervous system, the degree of intrinsic mitochondrial-mediated apoptotic signaling expresses a cell's individual metabolic stress, whereas activation of the extrinsic death receptor-induced cascade is regarded as a sign of imbalanced cellular networks. Under physiological conditions, most neurons possess death receptors without being sensitive to receptor-mediated apoptosis. This paradox raises two questions: what is the evolutionary advantage of expressing potentially harmful proteins? How is their signaling controlled? This review summarizes the functional relevance of FasL-Fas signaling--a quintessential death ligand/receptor system--in different neurological disease models ranging from traumatic, inflammatory and ischemic to neurodegenerative processes. Furthermore, it outlines alternative non-apoptotic Fas signaling, shedding new light on its neuroplastic capacity. Finally, receptor-proximal regulatory proteins are introduced and identified as potential protagonists of disease-modifying neurological therapies.

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Crosslinks between neuronal plasticity and death have been described for CD95 (Apo1/Fas).
“Crosslinks between neuronal plasticity and death have also been described for CD95 (Apo1/Fas).”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [96]
In neurons and neural precursor cells, CD95 is not a death receptor.
“In neurons and neural precursor cells, CD95 is not a death receptor.96”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [96]
Neural surface receptors integrate signals with diverse functions, such as neuronal injury and repair, and depending on pathophysiological context could have Janus-like roles in the ischaemic brain.
“Neural surface receptors integrate signals with diverse functions, such as neuronal injury and repair,96 which depending on the pathophysiological context could have Janus-like roles in the ischaemic brain.5,100”
From Promoting brain remodelling and plasticity for stroke recovery: therapeutic promise and potential pitfalls of clinical translation (2012) · cites this paper as [96]

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Authors: Reich, A., Spering, C., & Schulz, J. B.
Affiliations: University of Göttingen (DE)
Corresponding author: Schulz, Jörg B.
ORCID: Reich, Arno
Spering, Christopher
Schulz, Jörg B.
Venue: Trends in Neurosciences
Publisher: Elsevier BV
Published: 2008-09
Volume: 31
Issue: 9
Pages: 478-486
ISSN: 0166-2236 (ISSN-L)
DOI: 10.1016/j.tins.2008.06.007
OpenAlex: W2008584595
Cited by: 46
References: 70
Citations by year: 2022: 2 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 2 · 2016: 3 · 2015: 2 · 2014: 1 · 2013: 6 · 2012: 7
FWCI: 0.46
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Trends in Neurosciences (publishedVersion)
PubMed (publishedVersion)
Funders: Deutsche Forschungsgemeinschaft
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: Fas/CD95, Fas ligand, death receptor signaling, neuroplasticity, apoptosis, traumatic brain injury, neuroinflammation, cerebral ischemia, neurodegeneration, mitochondrial apoptosis, disease-modifying therapy
MeSH terms: Animals, Central Nervous System, Humans, Neuronal Plasticity, Signal Transduction, Antigens, CD, Apoptosis, Fas Ligand Protein

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Death receptor Fas (CD95) signaling in the central nervous system: tuning neuroplasticity?

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