eISSN: 1897-4252
ISSN: 1731-5530
Kardiochirurgia i Torakochirurgia Polska/Polish Journal of Thoracic and Cardiovascular Surgery
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2/2022
vol. 19
 
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Letter to the Editor

Can the development of lung fibrosis be prevented after COVID-19 infection?

Serdar Kalemci
1
,
Arife Zeybek
2
,
Ahmet Bulent Kargi
3

  1. Department of Anesthesia, Kocaeli University of Health and Technology, European Vocational School, Kocaeli, Turkey
  2. Department of Chest Surgery, Mugla Sitki Kocman University, Mugla, Turkey
  3. Department of Chest Surgery, Okan University, Istanbul, Turkey
Kardiochirurgia i Torakochirurgia Polska 2022; 19 (2): 113
Online publish date: 2022/06/29
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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) increases the expression of host cell surface receptors, either directly or through activation of host signaling. In this way, a cytokine storm can occur. It uses the ACE2 receptor for entry. ACE2 is the regulator of the renin-angiotensin system (RAS) and RAS is responsible for hemostatic balance through a balance of ACE and ACE2 activity. ACE produces angiotensin II as well as aldosterone release. Angiotensin II activates a wide variety of signaling pathways. Interleukin (IL)-6 can induce tumor necrosis factor-(TNF-) activation 6 and increased recruitment of neutrophils and macrophages as well as direct endothelial cell damage. It has also been shown to support collagen I gene activation through MAPK/ERK and transforming growth factor-(TGF-), which are critical factors in the fibrotic response. Thus, SARS-CoV-2 contributes to the activation of host profibrotic pathways [1]. Thymoquinone (TQ) is a bioactive component obtained from Nigella sativa. TQ has demonstrated antibacterial, anti-inflammatory, anti-oxidant, neuroprotective and antiapoptotic effects [2]. In addition, it has been shown that opioid-active peptides such as hemorphins are activated by TQ and thus have an inhibitory effect on ACE receptors [3]. Therefore, TQ can block SARS-CoV-2 entry by blocking the ACE2 receptor. In experimental studies, it has been shown that TQ blocks cytokine release by inhibiting NF-kB, reduces oxidative stress, and thus protects against lung fibrosis [4]. The anti-inflammatory, immunomodulatory and antifibrotic effects of macrolide antibiotics by blocking the MAPK signal chain have been demonstrated in lung fibrosis models [5]. Treatment of patient groups with a high risk of developing lung fibrosis (advanced age, history of intensive care hospitalization, long-term oxygen need, etc.) after COVID-19 infection with TQ or macrolide antibiotics may be protective against lung fibrosis. For these reasons, further clinical studies are required.

Disclosure

The authors report no conflict of interest.

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