SARS-CoV-2 and pathological matrix remodeling mediators

Imen Guizani, Nesrine Fourti, Wiem Zidi, Moncef Feki, Monia Allal-Elasmi, Imen Guizani, Nesrine Fourti, Wiem Zidi, Moncef Feki, Monia Allal-Elasmi

Abstract

Background: Recognizing only sharp elevation in a short period of time, the COVID-19 SARS-CoV-2 propagation is more and more marked in the whole world. Induced inflammation afterwards infection engenders a high infiltration of immune cells and cytokines that triggers matrix metalloproteinases (MMPs) activation. These endopeptidases are mediators of the lung extracellular matrix (ECM), a basic element for alveoli structure and gas exchange.

Methods: When immune cells, MMPs, secreted cytokines and several other mediators are gathered a pathological matrix remodeling occurs. This phenomenon tends to tissue destruction in the first place and a pulmonary hypertrophy and fibrosis in the second place.

Findings: After pathological matrix remodeling establishment, pathological diseases take place even after infection state. Since post COVID-19 pulmonary fibrosis is an emerging complication of the disease, there is an urge to better understand and characterize the implication of ECM remodeling during SARS-CoV-2 infection.

Conclusion: Targeting MMPs and their inhibitors could be a probable solution for occurred events since there are many cured patients that remain with severe sequels even after the end of infection.

Keywords: Cytokine; Immune cells; MMPs; Matrix remodeling; SARS-CoV-2; Therapeutic target.

Conflict of interest statement

The authors declare that they have no conflict of interest and no financial support regarding this review project.

© 2021. The Author(s), under exclusive licence to Springer Nature Switzerland AG.

Figures

Fig. 1
Fig. 1
Induced pathological matrix remodeling after SARS-CoV-2 infection. A Cell entry mechanism of SARS-CoV-2 summary: the initial step of SARS-CoV-2 infection involves a specific binding of S-protein to host cell entry receptors, angiotensin-converting enzyme 2 (ACE2). Gathered together and with the host cell surface serine protease TMPRSS2, the entry process is activated. Following the endocytosis, cathepsins are released. These proteases modify once again the S-protein and promote the release of viral RNA into the cytoplasm. B SARS-CoV-2 Physio-pathological implications: when virus propagation occurs, a massive destruction of tissues takes place. An epithelial damage is the initial hallmark of SARS-CoV-2 infection. A specific immune response is induced to eliminate the virus and initiate the inflammatory response. The immune cells, in particular, macrophages identify the virus and release pro-inflammatory mediators (cytokines, chemokines, growth factors…). Cytokines activate more immune cells, which in turn produce more cytokines creating an uncontrolled cycle of inflammatory response “cytokine storm”. Activated immune and non-immune cells produce MMPs which lead to ECM breakdown disruption and this unresolved infection gives rise to damages. These damages do happen during the cytokine storm which includes the unbalance of the MMPs/TIMPs ratio, the increase deposition of ECM fragments, and the massive formation and deposition of fibrin. ACE2 angiotensin-converting enzyme 2, ADAM-17 ADAM metalloprotease domain 17, Cat L cathepsin L, Cat B cathepsin B, TMPRSS2 transmembrane protease serine 2, DC dendritic cell, MMPs matrix metalloproteinases, MT-MMPs membrane-type matrix metalloproteinases, TIMPs tissue inhibitors of matrix metalloproteinases
Fig. 2
Fig. 2
ECM lung evolution from healthy to a pathological matrix. A Healthy lung matrix structure is preserved by the presence of fibroblasts, collagen, elastin and anchored fibronectin to basal membrane. B ECM breakdown after virus infiltration and MMP overexpression (from day 1 to 5 of infection): collagen fibers destruction through secreted MMPs by inflammatory cells. This destruction leads to basement membrane disruption. C ECM lungs fibrosis and hypertrophy (from day 5 of infection and more): after increased degradation, a remodeling takes place to respond to lung injuries. However, ECM mediators’ imbalance and SMC migration lead to increased collagens and matrix degradation products deposition that are presumed in a thickened matrix. SARS-CoV-2 severe acute respiratory syndrome coronavirus-2, MMP matrix metalloproteinase, TIMP tissue inhibitor of matrix metalloproteinase, ECM extracellular matrix, SMC smooth muscle cells, DC dendritic cells
Fig. 3
Fig. 3
Targeting ECM mediators as a therapeutic solution after SARS-CoV-2 infection could prevent from severe complications: matrix equilibrium is primordial for maintaining a healthy lung structure, when MMP/TIMP ration is in favor of MMPs, a matrix destruction occurs and when it is in favor of TIMPs a thickened matrix is observed. MMP matrix metalloproteinase, TIMP tissue inhibitor of matrix metalloproteinase, ECM extracellular matrix

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