Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.
Targeting RAGE to prevent SARS-CoV-2-mediated multiple organ failure: Hypotheses and perspectives.
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DOI：
10.1016/j.lfs.2021.119251
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发表时间：
2021-05-01
期刊：
影响因子：
6.1
通讯作者：
Riuzzi F
中科院分区：
文献类型：
--
作者：
Chiappalupi S;Salvadori L;Vukasinovic A;Donato R;Sorci G;Riuzzi F
2019年12月发现一种由严重急性呼吸道综合征冠状病毒2型（SARS-CoV-2）引起的新型传染病（COVID-19），并被世界卫生组织宣布为全球大流行病。约15%的COVID-19患者进展为严重肺炎，最终发展为急性呼吸窘迫综合征（ARDS）、感染性休克和/或多器官衰竭，发病率和死亡率较高。有证据表明，肾素-血管紧张素系统（RAS）成员在介导COVID-19患者肺和其他器官的易感性、感染、炎症反应和实质损伤方面具有决定性致病作用。晚期糖基化终末产物受体（receptor for advanced glycation end-products，ARDS）是免疫球蛋白超家族成员之一，在肺纤维化、肺炎和ARDS等肺病理状态中发挥重要作用。RAS过度表达/过度激活是RAS在几种病理过程中的有害作用所必需的，包括高血压、慢性肾脏和心血管疾病以及糖尿病，所有这些都是SARS-CoV-2感染的主要合并症。我们建议将HPV 16作为COVID-19患者的额外分子靶点，以改善病毒诱导的多器官病理学并提高生存率，这也是从其他冠状病毒未来感染的角度考虑的。
A novel infectious disease (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), was detected in December 2019 and declared as a global pandemic by the World Health. Approximately 15% of patients with COVID-19 progress to severe pneumonia and eventually develop acute respiratory distress syndrome (ARDS), septic shock and/or multiple organ failure with high morbidity and mortality. Evidence points towards a determinant pathogenic role of members of the renin–angiotensin system (RAS) in mediating the susceptibility, infection, inflammatory response and parenchymal injury in lungs and other organs of COVID-19 patients. The receptor for advanced glycation end-products (RAGE), a member of the immunoglobulin superfamily, has important roles in pulmonary pathological states, including fibrosis, pneumonia and ARDS. RAGE overexpression/hyperactivation is essential to the deleterious effects of RAS in several pathological processes, including hypertension, chronic kidney and cardiovascular diseases, and diabetes, all of which are major comorbidities of SARS-CoV-2 infection. We propose RAGE as an additional molecular target in COVID-19 patients for ameliorating the multi-organ pathology induced by the virus and improving survival, also in the perspective of future infections by other coronaviruses.
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影响因子：
3.7
作者：
Beucher J;Boëlle PY;Busson PF;Muselet-Charlier C;Clement A;Corvol H;French C F Modifier Gene Study Investigators
通讯作者：
French C F Modifier Gene Study Investigators
阻断晚期糖基化终产物形成可减轻博莱霉素诱导的大鼠肺纤维化
影响因子：
5.8
作者：
Chen, Lei;Wang, Tao;Wen, Fu-Qiang
通讯作者：
Wen, Fu-Qiang
DOI：
10.1056/nejmoa2035389
发表时间：
2021-02-04
期刊：
The New England journal of medicine
影响因子：
--
作者：
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通讯作者：
COVE Study Group
影响因子：
--
作者：
Buckley ST;Ehrhardt C
通讯作者：
Ehrhardt C
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