Dicarbonyl stress is a dysfunctional state consisting in the abnormal accumulation of reactive α-oxaldehydes leading to increased protein modification. In cells, post-translational changes can also occur through S-glutathionylation, a highly conserved oxidative post-translational modification consisting of the formation of a mixed disulfide between glutathione and a protein cysteine residue. This review recapitulates the main findings supporting a role for dicarbonyl stress and S-glutathionylation in the pathogenesis of cerebrovascular diseases, with specific emphasis on cerebral cavernous malformations (CCM), a vascular disease of proven genetic origin that may give rise to various clinical signs and symptoms at any age, including recurrent headaches, seizures, focal neurological deficits, and intracerebral hemorrhage. A possible interplay between dicarbonyl stress and S-glutathionylation in CCM is also discussed.

Dicarbonyl stress and s-glutathionylation in cerebrovascular diseases: A focus on cerebral cavernous malformations

Perrelli A.;Retta S. F.
2020

Abstract

Dicarbonyl stress is a dysfunctional state consisting in the abnormal accumulation of reactive α-oxaldehydes leading to increased protein modification. In cells, post-translational changes can also occur through S-glutathionylation, a highly conserved oxidative post-translational modification consisting of the formation of a mixed disulfide between glutathione and a protein cysteine residue. This review recapitulates the main findings supporting a role for dicarbonyl stress and S-glutathionylation in the pathogenesis of cerebrovascular diseases, with specific emphasis on cerebral cavernous malformations (CCM), a vascular disease of proven genetic origin that may give rise to various clinical signs and symptoms at any age, including recurrent headaches, seizures, focal neurological deficits, and intracerebral hemorrhage. A possible interplay between dicarbonyl stress and S-glutathionylation in CCM is also discussed.
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https://www.mdpi.com/2076-3921/9/2/124/pdf
https://www.ncbi.nlm.nih.gov/pubmed/32024152
Advanced glycation end products; Cerebral cavernous malformations; Cerebrovascular disease; Dicarbonyl stress; Glutathione; Glyoxalase 1; Methylglyoxal; Oxidative stress; S-glutathionylation
Antognelli C.; Perrelli A.; Armeni T.; Talesa V.N.; Retta S.F.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2318/1729932
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