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An Open Question: Is It Rational to Inhibit the mTor-Dependent Pathway as COVID-19 Therapy?
G. Terrazzano, V. Rubino, A. T. Palatucci, A. Giovazzino, F. Carriero, G. Ruggiero
In December 2019, a novel coronavirus infection appeared in China (Wuhan City and Hubei Province), causing the first cases of abnormal severe pneumonia. Since then, the SARS-Cov2 infection has become pandemic and the correlated coronavirus disease (…
In December 2019, a novel coronavirus infection appeared in China (Wuhan City and Hubei Province), causing the first cases of abnormal severe pneumonia. Since then, the SARS-Cov2 infection has become pandemic and the correlated coronavirus disease (COVID-19) has been showing a plethora of pathophysiological manifestations that do not exclusively reduce COVID-19 to the occurrence of severe acute respiratory distress (Cevik et al., 2020; Chen et al., 2020; Harapan et al., 2020; Ryu and Chun, 2020; Sen et al., 2020). Although the immunological responses against SARS-Cov2 remain poorly defined (Chen et al., 2020; Li et al., 2020; Nikolich-Zugich et al., 2020; Qin et al., 2020), it is of note that the critical phase of COVID-19 currently appears, at least in some critical pathophysiological aspects, as a sort of autoimmune disease or as immune response hypersensitivity. Consequently, many authors have proposed various therapeutic approaches based on the modulation/inhibition of abnormal immune response in COVID-19 (Askanase et al., 2020; Chen et al., 2020; Geng et al., 2020; Li et al., 2020; Nikolich-Zugich et al., 2020; Piva et al., 2020; Qin et al., 2020; Radbel et al., 2020; Whyte et al., 2020; Ye et al., 2020; Yuki et al., 2020; Zhao, 2020). Recently, the effects of Tocilizumab administration has seemed to indicate that inhibition of the Interleukin (IL)-6 receptor (IL-6R) may result in the recovery of critical COVID-19 patients (Aziz et al., 2020; Zhang et al., 2020) in the advanced post-alveolitic phase, when extensive pulmonary fibrosis is accompanied by a diffuse interstitial inflammation apparently sustained by a described exacerbated cytokine storm (Askanase et al., 2020; Chen et al., 2020; Geng et al., 2020; Li et al., 2020; Nikolich-Zugich et al., 2020; Piva et al., 2020; Qin et al., 2020; Radbel et al., 2020; Whyte et al., 2020; Ye et al., 2020; Yuki et al., 2020; Zhao, 2020). Such evidence highlights the critical relevance of controlling the IL-6/IL-6R pro-inflammatory pathway in the pathophysiology of COVID-19 in order to mitigate the adverse immune response that is a determinant of the most serious and undesirable phase of SARS-Cov2 infection (Whyte et al., 2020; Yuki et al., 2020; Zhao, 2020). In particular, hyper-reactivity was described as a major feature of the critical phase of COVID-19, broadly due to the hyperacute inflammatory context that leads to pulmonary interstitial disease and severe acute respiratory distress (Askanase et al., 2020; Chen et al., 2020; Geng et al., 2020; Li et al., 2020; Nikolich-Zugich et al., 2020; Piva et al., 2020; Qin et al., 2020; Radbel et al., 2020; Whyte et al., 2020; Ye et al., 2020; Yuki et al., 2020; Zhao, 2020).
Published in
Frontiers in Pharmacology
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4
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5 | 2020 |
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