COVID-19, ferrosenescence and neurodegeneration, a mini-review.
Prog Neuropsychopharmacol Biol Psychiatry
; 109: 110230, 2021 07 13.
Article
in English
| MEDLINE | ID: covidwho-989032
ABSTRACT
Exacerbation of cognitive, motor and nonmotor symptoms have been described in critically ill COVID-19 patients, indicating that, like prior pandemics, neurodegenerative sequelae may mark the aftermath of this viral infection. Moreover, SARS-CoV-2, the causative agent of COVID-19 disease, was associated with hyperferritinemia and unfavorable prognosis in older individuals, suggesting virus-induced ferrosenescence. We have previously defined ferrosenescence as an iron-associated disruption of both the human genome and its repair mechanisms, leading to premature cellular senescence and neurodegeneration. As viruses replicate more efficiently in iron-rich senescent cells, they may have developed the ability to induce this phenotype in host tissues, predisposing to both immune dysfunction and neurodegenerative disorders. In this mini-review, we summarize what is known about the SARS-CoV-2-induced cellular senescence and iron dysmetabolism. We also take a closer look at immunotherapy with natural killer cells, angiotensin II receptor blockers ("sartans"), iron chelators and dipeptidyl peptidase 4 inhibitors ("gliptins") as adjunct treatments for both COVID-19 and its neurodegenerative complications.
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Cellular Senescence
/
Iron Metabolism Disorders
/
Neurodegenerative Diseases
/
COVID-19
Type of study:
Prognostic study
Topics:
Long Covid
Limits:
Humans
Language:
English
Journal:
Prog Neuropsychopharmacol Biol Psychiatry
Year:
2021
Document Type:
Article
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