Abstract
Original language | English |
---|---|
Pages (from-to) | 33-37 |
Number of pages | 5 |
Journal | Cytokine Growth Factor Rev. |
Volume | 53 |
DOIs | |
Publication status | Published - 2020 |
Keywords
- Cardiovascular diseases
- COVID-19
- Host-directed therapies
- Inflamm-aging
- interleukin-6
- SARS-CoV-2
- angiotensin converting enzyme 2
- antivirus agent
- interferon
- dipeptidyl carboxypeptidase
- IL6 protein, human
- interleukin 6
- monoclonal antibody
- tocilizumab
- adverse outcome
- Article
- biological phenomena and functions concerning the entire organism
- cardiovascular disease
- chronic disease
- chronic inflammation
- comorbidity
- coronavirus disease 2019
- cytokine release syndrome
- disease severity
- down regulation
- enzyme activity
- enzyme defect
- enzyme regulation
- geriatric disorder
- high risk population
- human
- immune response
- immunopathology
- immunosenescence
- inflammation
- male
- mortality
- mortality rate
- nonhuman
- priority journal
- Severe acute respiratory syndrome coronavirus 2
- systemic disease
- virus cell interaction
- aged
- aging
- Betacoronavirus
- biosynthesis
- blood
- Coronavirus infection
- female
- immunology
- metabolism
- pandemic
- pathology
- severe acute respiratory syndrome
- very elderly
- virus pneumonia
- Aged
- Aged, 80 and over
- Aging
- Antibodies, Monoclonal, Humanized
- Comorbidity
- Coronavirus Infections
- Female
- Humans
- Inflammation
- Interferon Type I
- Interleukin-6
- Male
- Pandemics
- Peptidyl-Dipeptidase A
- Pneumonia, Viral
- Severe Acute Respiratory Syndrome
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Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes : Cytokine and Growth Factor Reviews. / Bonafè, M.; Prattichizzo, F.; Giuliani, A. et al.
In: Cytokine Growth Factor Rev., Vol. 53, 2020, p. 33-37.Research output: Contribution to journal › Article › peer-review
}
TY - JOUR
T1 - Inflamm-aging: Why older men are the most susceptible to SARS-CoV-2 complicated outcomes
T2 - Cytokine and Growth Factor Reviews
AU - Bonafè, M.
AU - Prattichizzo, F.
AU - Giuliani, A.
AU - Storci, G.
AU - Sabbatinelli, J.
AU - Olivieri, F.
N1 - Cited By :30 Export Date: 5 March 2021 CODEN: CGFRF Correspondence Address: Prattichizzo, F.; IRCCS MultiMedica, Via Fantoli 16/15, Italy; email: francesco.prattichizzo@multimedica.it Correspondence Address: Giuliani, A.; Department of Clinical and Molecular Sciences, Via Tronto 10/A, Italy; email: angelica.giuliani@staff.univpm.it Chemicals/CAS: dipeptidyl carboxypeptidase, 9015-82-1; tocilizumab, 375823-41-9; angiotensin converting enzyme 2; Antibodies, Monoclonal, Humanized; IL6 protein, human; Interferon Type I; Interleukin-6; Peptidyl-Dipeptidase A; tocilizumab Funding details: Università Politecnica delle Marche, UNIVPM Funding text 1: This work was supported by the I talian Ministry of Health [Ricerca Corrente grants to IRCCS MultiMedica] and by Università Politecnica delle Marche (UNIVPM) [RSA grants to F.O.]. 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PY - 2020
Y1 - 2020
N2 - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that four well-recognized features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men: i. the presence of subclinical systemic inflammation without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation; iii. the downregulation of ACE2 (i.e. the SARS-CoV-2 receptor); and iv. accelerated biological aging. The high mortality rate of SARS-CoV-2 infection suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection. © 2020 Elsevier Ltd
AB - Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is characterized by a high mortality of elderly men with age-related comorbidities. In most of these patients, uncontrolled local and systemic hyperinflammation induces severe and often lethal outcomes. The aging process is characterized by the gradual development of a chronic subclinical systemic inflammation (inflamm-aging) and by acquired immune system impairment (immune senescence). Here, we advance the hypothesis that four well-recognized features of aging contribute to the disproportionate SARS-CoV-2 mortality suffered by elderly men: i. the presence of subclinical systemic inflammation without overt disease, ii. a blunted acquired immune system and type I interferon response due to the chronic inflammation; iii. the downregulation of ACE2 (i.e. the SARS-CoV-2 receptor); and iv. accelerated biological aging. The high mortality rate of SARS-CoV-2 infection suggests that clarification of the mechanisms of inflamm-aging and immune senescence can help combat not only age-related disorders but also SARS-CoV-2 infection. © 2020 Elsevier Ltd
KW - Cardiovascular diseases
KW - COVID-19
KW - Host-directed therapies
KW - Inflamm-aging
KW - interleukin-6
KW - SARS-CoV-2
KW - angiotensin converting enzyme 2
KW - antivirus agent
KW - interferon
KW - dipeptidyl carboxypeptidase
KW - IL6 protein, human
KW - interleukin 6
KW - monoclonal antibody
KW - tocilizumab
KW - adverse outcome
KW - Article
KW - biological phenomena and functions concerning the entire organism
KW - cardiovascular disease
KW - chronic disease
KW - chronic inflammation
KW - comorbidity
KW - coronavirus disease 2019
KW - cytokine release syndrome
KW - disease severity
KW - down regulation
KW - enzyme activity
KW - enzyme defect
KW - enzyme regulation
KW - geriatric disorder
KW - high risk population
KW - human
KW - immune response
KW - immunopathology
KW - immunosenescence
KW - inflammation
KW - male
KW - mortality
KW - mortality rate
KW - nonhuman
KW - priority journal
KW - Severe acute respiratory syndrome coronavirus 2
KW - systemic disease
KW - virus cell interaction
KW - aged
KW - aging
KW - Betacoronavirus
KW - biosynthesis
KW - blood
KW - Coronavirus infection
KW - female
KW - immunology
KW - metabolism
KW - pandemic
KW - pathology
KW - severe acute respiratory syndrome
KW - very elderly
KW - virus pneumonia
KW - Aged
KW - Aged, 80 and over
KW - Aging
KW - Antibodies, Monoclonal, Humanized
KW - Comorbidity
KW - Coronavirus Infections
KW - Female
KW - Humans
KW - Inflammation
KW - Interferon Type I
KW - Interleukin-6
KW - Male
KW - Pandemics
KW - Peptidyl-Dipeptidase A
KW - Pneumonia, Viral
KW - Severe Acute Respiratory Syndrome
U2 - 10.1016/j.cytogfr.2020.04.005
DO - 10.1016/j.cytogfr.2020.04.005
M3 - Article
SN - 1359-6101
VL - 53
SP - 33
EP - 37
JO - Cytokine Growth Factor Rev.
JF - Cytokine Growth Factor Rev.
ER -