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Review
. 2022 May 26;14(6):1135.
doi: 10.3390/pharmaceutics14061135.

Post-COVID Syndrome: The Research Progress in the Treatment of Pulmonary sequelae after COVID-19 Infection

Valentina Ruggiero  1   2 , Rita P Aquino  1 , Pasquale Del Gaudio  1 , Pietro Campiglia  1 , Paola Russo  1
Affiliations
Review

Post-COVID Syndrome: The Research Progress in the Treatment of Pulmonary sequelae after COVID-19 Infection

Valentina Ruggiero et al. Pharmaceutics. .

Abstract

Post-COVID syndrome or long COVID is defined as the persistence of symptoms after confirmed SARS-CoV-2 infection, the pathogen responsible for coronavirus disease. The content herein presented reviews the reported long-term consequences and aftereffects of COVID-19 infection and the potential strategies to adopt for their management. Recent studies have shown that severe forms of COVID-19 can progress into acute respiratory distress syndrome (ARDS), a predisposing factor of pulmonary fibrosis that can irreversibly compromise respiratory function. Considering that the most serious complications are observed in the airways, the inhalation delivery of drugs directly to the lungs should be preferred, since it allows to lower the dose and systemic side effects. Although further studies are needed to optimize these techniques, recent studies have also shown the importance of in vitro models to recreate the SARS-CoV-2 infection and study its sequelae. The information reported suggests the necessity to develop new inhalation therapies in order to improve the quality of life of patients who suffer from this condition.

Keywords: in vitro lung models; inhalation therapy; long COVID; post-COVID fibrosis; post-COVID sequelae; post-COVID syndrome.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Long-term consequences and aftereffects of COVID-19 infections.
Figure 2
Figure 2
Interaction between SARS-CoV-2 and the Renin–Angiotensin System. SARS-CoV-2 enters host cells through the interaction of its spike protein with the ACE2 receptor. The downregulation of ACE2 receptors results in a decrease in the cleavage of angiotensin I and angiotensin II at Ang 1–9 and Ang 1–7, respectively. Ang II, through interaction with the AT1R receptor, stimulates the gene expression of various inflammatory cytokines and also influences the activation of macrophages that contribute to the “cytokine storm”.
Figure 3
Figure 3
Key events in the progression of cytokine storm to acute respiratory distress syndrome (ARDS) and pulmonary fibrosis.
Figure 4
Figure 4
Schematic representation of the lung-on-chip device: in the microchannel in red flows a liquid similar to blood, in the blue one the air flows.
See this image and copyright information in PMC

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