Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients.
Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients.
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DOI：
10.1016/j.bcp.2021.114812
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发表时间：
2021-11
影响因子：
5.8
通讯作者：
Martini C
中科院分区：
文献类型：
--
作者：
Giacomelli C;Piccarducci R;Marchetti L;Romei C;Martini C
肺纤维化（PF）的特征是肺泡间隙内的多种级别的慢性炎症和胶原沉积，是间质性肺疾病（ILD）的标志。最近，传染源已成为 PF 发展的驱动因素；然而，病毒/细菌感染在 PF 发生和传播中的作用仍存在争议。在这种情况下，导致当前 2019 年冠状病毒病 (COVID-19) 大流行的严重急性呼吸综合征冠状病毒 2 (SARS-CoV-2) 与急性呼吸窘迫综合征 (ARDS) 和 PF 的发展有关。尽管在大多数情况下可以根除 SARS-CoV-2 感染，但不能排除纤维化病变的发展；此外，这些病变是稳定的还是进行性纤维化事件仍不清楚。本文概述了驱动纤维化过程的主要分子机制以及目前批准的和新提出的治疗解决方案。然后，讨论了来自 COVID-19 后患者的最新数据，以比较 PF 和 COVID-19 依赖性 PF，强调共同和特定的机制。当然需要更好地了解 PF 病因，同时也需要制定有效的治疗策略，而 COVID-19 病理学为实现这一目标提供了又一个机会。总的来说，这里报告的工作可能有助于定义针对 ILD 谱系多样性的治疗干预的新方法。
Pulmonary fibrosis (PF) is characterised by several grades of chronic inflammation and collagen deposition in the interalveolar space and is a hallmark of interstitial lung diseases (ILDs). Recently, infectious agents have emerged as driving causes for PF development; however, the role of viral/bacterial infections in the initiation and propagation of PF is still debated. In this context, the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus responsible for the current coronavirus disease 2019 (COVID-19) pandemic, has been associated with acute respiratory distress syndrome (ARDS) and PF development. Although the infection by SARS-CoV-2 can be eradicated in most cases, the development of fibrotic lesions cannot be precluded; furthermore, whether these lesions are stable or progressive fibrotic events is still unknown. Herein, an overview of the main molecular mechanisms driving the fibrotic process together with the currently approved and newly proposed therapeutic solutions was given. Then, the most recent data that emerged from post-COVID-19 patients was discussed, in order to compare PF and COVID-19-dependent PF, highlighting shared and specific mechanisms. A better understanding of PF aetiology is certainly needed, also to develop effective therapeutic strategies and COVID-19 pathology is offering one more chance to do it. Overall, the work reported here could help to define new approaches for therapeutic intervention in the diversity of the ILD spectrum.
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