tetano
Editor, Senior Moderator
Biochem Pharmacol
. 2021 Oct 20;114812.
doi: 10.1016/j.bcp.2021.114812. Online ahead of print.
Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients
Chiara Giacomelli[SUP] 1 [/SUP], Rebecca Piccarducci[SUP] 1 [/SUP], Laura Marchetti[SUP] 1 [/SUP], Chiara Romei[SUP] 2 [/SUP], Claudia Martini[SUP] 3 [/SUP]
Affiliations
Abstract
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.
Keywords: Interstitial Lung Disease; Myofibroblast; Pulmonary fibrosis; SARS-CoV-2 severe acute respiratory syndrome coronavirus 2.
. 2021 Oct 20;114812.
doi: 10.1016/j.bcp.2021.114812. Online ahead of print.
Pulmonary fibrosis from molecular mechanisms to therapeutic interventions: lessons from post-COVID-19 patients
Chiara Giacomelli[SUP] 1 [/SUP], Rebecca Piccarducci[SUP] 1 [/SUP], Laura Marchetti[SUP] 1 [/SUP], Chiara Romei[SUP] 2 [/SUP], Claudia Martini[SUP] 3 [/SUP]
Affiliations
- PMID: 34687672
- DOI: 10.1016/j.bcp.2021.114812
Abstract
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.
Keywords: Interstitial Lung Disease; Myofibroblast; Pulmonary fibrosis; SARS-CoV-2 severe acute respiratory syndrome coronavirus 2.