Abstract
Elastin represents the structural component of the extracellular matrix providing elastic recoil to tissues such as skin, blood vessels and lungs. Elastogenic cells secrete soluble tropoelastin monomers into the extracellular space where these monomers associate with other matrix proteins (e.g., microfibrils and glycoproteins) and are crosslinked by lysyl oxidase to form insoluble fibres. Once elastic fibres are formed, they are very stable, highly resistant to degradation and have an almost negligible turnover. However, there are circumstances, mainly related to inflammatory conditions, where increased proteolytic degradation of elastic fibres may lead to consequences of major clinical relevance. In severely affected COVID-19 patients, for instance, the massive recruitment and activation of neutrophils is responsible for the profuse release of elastases and other proteolytic enzymes which cause the irreversible degradation of elastic fibres. Within the lungs, destruction of the elastic network may lead to the permanent impairment of pulmonary function, thus suggesting that elastases can be a promising target to preserve the elastic component in COVID-19 patients. Moreover, intrinsic and extrinsic factors additionally contributing to damaging the elastic component and to increasing the spread and severity of SARS-CoV-2 infection are reviewed.
Highlights
Since the dramatic spread of the severe acute respiratory coronavirus virus 2 (SARSCoV-2)-induced pandemic, an exponentially increased number of investigations have been performed to better understand the pathogenic mechanisms, clinical manifestations as well as possible preventive and therapeutic strategies
Severe COVID19 pathophysiology is characterized by altered neutrophil quantity, phenotype and functioning in the blood as well as in the lungs [119], where neutrophils contribute to the proteolytic damage of tissue elasticity through a disproportionate release of virus-induced neutrophil extracellular traps (NETs) [120]
Elastic Fibres and Elastases in SARS-CoV-2 Infection In COVID-19 patients, neutrophils are the major source of elastases, which are stored in cytoplasmic granules and are released upon neutrophil activation as part of an inflammatory response to viral infection [148]
Summary
Since the dramatic spread of the severe acute respiratory coronavirus virus 2 (SARSCoV-2)-induced pandemic, an exponentially increased number of investigations have been performed to better understand the pathogenic mechanisms, clinical manifestations as well as possible preventive and therapeutic strategies. Despite the clear evidence that lungs are primarily involved, only few reports have emphasized the impact of this infection on the extracellular compartment of the lung parenchyma. Within this context, elastic fibres represent the extracellular component exhibiting the greatest flexibility since they are capable of being extended up to 230% of their unloaded length without rupture [1]. The aim of the present review is to update and explore the current knowledge on elastic fibres, on their fate in coronavirus disease-19 (COVID-19) patients and on the therapeutic options that, limiting/inhibiting elastolytic activities, may preserve the morpho-functional properties of the lungs.
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