Age-related mitochondrial dysfunction as a key factor in COVID-19 disease.
Age-related mitochondrial dysfunction as a key factor in COVID-19 disease.
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DOI:
10.1016/j.exger.2020.111147
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发表时间:
2020-12
影响因子:
3.9
通讯作者:
López-Lluch G
中科院分区:
文献类型:
--
作者:
Moreno Fernández-Ayala DJ;Navas P;López-Lluch G
SARS-CoV-2 causes a severe pneumonia (COVID-19) that affects essentially elderly people. In COVID-19, macrophage infiltration into the lung causes a rapid and intense cytokine storm leading finally to a multi-organ failure and death. Comorbidities such as metabolic syndrome, obesity, type 2 diabetes, lung and cardiovascular diseases, all of them age-associated diseases, increase the severity and lethality of COVID-19. Mitochondrial dysfunction is one of the hallmarks of aging and COVID-19 risk factors. Dysfunctional mitochondria is associated with defective immunological response to viral infections and chronic inflammation. This review discuss how mitochondrial dysfunction is associated with defective immune response in aging and different age-related diseases, and with many of the comorbidities associated with poor prognosis in the progression of COVID-19. We suggest here that chronic inflammation caused by mitochondrial dysfunction is responsible of the explosive release of inflammatory cytokines causing severe pneumonia, multi-organ failure and finally death in COVID-19 patients. Preventive treatments based on therapies improving mitochondrial turnover, dynamics and activity would be essential to protect against COVID-19 severity. Mitochondrial dysfunction is associated with aging and age-related diseases and metabolic syndrome. Unbalanced activity of mitochondria is involved in inflammation and dysfunctional response to virus infection. COVID-19 severity is higher in aged and metabolic syndrome related diseases. Improvement of mitochondrial activity during aging can improve response to virus infections including respiratory virus. Reduction of dysfunctional mitochondria can reduce the inflammatory response to SARS-CoV-2 infection.
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DOI:
10.1126/science.abd4585
发表时间:
2020-10-23
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Bastard P;Rosen LB;Zhang Q;Michailidis E;Hoffmann HH;Zhang Y;Dorgham K;Philippot Q;Rosain J;Béziat V;Manry J;Shaw E;Haljasmägi L;Peterson P;Lorenzo L;Bizien L;Trouillet-Assant S;Dobbs K;de Jesus AA;Belot A;Kallaste A;Catherinot E;Tandjaoui-Lambiotte Y;Le Pen J;Kerner G;Bigio B;Seeleuthner Y;Yang R;Bolze A;Spaan AN;Delmonte OM;Abers MS;Aiuti A;Casari G;Lampasona V;Piemonti L;Ciceri F;Bilguvar K;Lifton RP;Vasse M;Smadja DM;Migaud M;Hadjadj J;Terrier B;Duffy D;Quintana-Murci L;van de Beek D;Roussel L;Vinh DC;Tangye SG;Haerynck F;Dalmau D;Martinez-Picado J;Brodin P;Nussenzweig MC;Boisson-Dupuis S;Rodríguez-Gallego C;Vogt G;Mogensen TH;Oler AJ;Gu J;Burbelo PD;Cohen JI;Biondi A;Bettini LR;D'Angio M;Bonfanti P;Rossignol P;Mayaux J;Rieux-Laucat F;Husebye ES;Fusco F;Ursini MV;Imberti L;Sottini A;Paghera S;Quiros-Roldan E;Rossi C;Castagnoli R;Montagna D;Licari A;Marseglia GL;Duval X;Ghosn J;HGID Lab;NIAID-USUHS Immune Response to COVID Group;COVID Clinicians;COVID-STORM Clinicians;Imagine COVID Group;French COVID Cohort Study Group;Milieu Intérieur Consortium;CoV-Contact Cohort;Amsterdam UMC Covid-19 Biobank;COVID Human Genetic Effort;Tsang JS;Goldbach-Mansky R;Kisand K;Lionakis MS;Puel A;Zhang SY;Holland SM;Gorochov G;Jouanguy E;Rice CM;Cobat A;Notarangelo LD;Abel L;Su HC;Casanova JL
通讯作者:
Casanova JL
DOI:
10.1097/mco.0000000000000444
发表时间:
2018-03
影响因子:
3.1
作者:
Beijers RJHCG;Gosker HR;Schols AMWJ
通讯作者:
Schols AMWJ
DOI:
10.1126/science.abc6261
发表时间:
2020-09-04
期刊:
Science (New York, N.Y.)
影响因子:
--
作者:
Arunachalam PS;Wimmers F;Mok CKP;Perera RAPM;Scott M;Hagan T;Sigal N;Feng Y;Bristow L;Tak-Yin Tsang O;Wagh D;Coller J;Pellegrini KL;Kazmin D;Alaaeddine G;Leung WS;Chan JMC;Chik TSH;Choi CYC;Huerta C;Paine McCullough M;Lv H;Anderson E;Edupuganti S;Upadhyay AA;Bosinger SE;Maecker HT;Khatri P;Rouphael N;Peiris M;Pulendran B
通讯作者:
Pulendran B
影响因子:
2.2
作者:
Anand SK;Tikoo SK
通讯作者:
Tikoo SK
影响因子:
64.8
作者:
Baur, Joseph A.;Pearson, Kevin J.;Sinclair, David A.
通讯作者:
Sinclair, David A.