Pulmonary Covid Fibrosis a New Pharmaceutic Approach

Roberto Menicagli, Mario Limodio, Marta Limodio, Maria Teresa Casotti, Laura Menicagli

Abstract


Background: Patient’s post‑COVID may develop chronic irreversible respiratory failure with “widespread signs of pulmonary fibrosis.” Our study analyzed the causes of this fibrosis to propose a therapeutic protocol.

Methods: Identification of the biochemical causes of fibrosis in COVID‑19 analysing the literature and chest CT.

Results: The CT imaging shows pulmonary fibrosis. The viral infection produces “interleukin‑6”, which binds to its receptor, in MUC1 of lung epithelial cells. The biochemical response of the cells promotes an over‑expression of MUC1 with fibrosis. Interleukin6 also causes a metabolic imbalance in NO that promotes clots and atherosclerosis of the pulmonary vessels. These results show to promote NO endothelia’s formation to block both the excessive expression of MUC1 and the atherosclerosis effect of the vessels.

Conclusions: This study proposes to inhibit phosphodiesterase by vasodilatation of the pulmonary vascular bed and the MUC1 over expression by interleukin6, the Sildenafil with the SGLT2 and N‑Acetylcysteine.


Keywords


COVID 19; fibrosis; lung

Full Text:

PDF

References


Zuo W, Zhao X, Chen Y G. SARS coronavirus and lung fibrosis.

Mol Biol SARS Coronavirus 2009:247-58. https://www.ncbi.

nlm.nih.gov/pmc/articles/PMC7176214/ Molecular Biology of

the SARS-Coronavirus. [Last accessed on 2009 Jul 22]. doi:

1007/978 3 642 03683 5_15.

George PM, Wells AU, Jenkins RG. Pulmonary fibrosis and

COVID 19: The potential role for antifibrotic therapy. Lancet

Respir Med 2020;8:807-15.

Isidori AM, Giannetta E, Pofi R, M.A. Venneri, D

Gianfrilli, F. Campolo, CM Mastroianni, A. Lenzi, and G.

d’Ettorre Targeting the NO‐cGMP‐PDE5 pathway in COVID‐19

infection Andrology. 2020: 10.1111/andr.12837.

Didion SP. Cellular and oxidative mechanisms associated

with interleukin 6 signaling in the vasculature. Int J Mol Sci

;18:2563.

Hung M J. Interleukin 6 inhibits endothelial nitric oxide synthase

activation and increases endothelial nitric oxide synthase binding

to stabilized caveolin 1 in human vascular endothelial cells. J

Hypertens 2010;28:940-51.

Ballester B, Milara J, Cortijo J. Mucins as a new frontier

inpulmonary fibrosis. J Clin Med 2019;8:1447.

Dal Moro F, Livi U. Any possible role of phosphodiesterase type

inhibitors in the treatment of severe COVID19 infections? A

lesson from urology. Clin Immunol 2020;214:108414.

Mondaini N. Phosphodiesterase type 5 inhibitors and COVID

: Are they useful in disease managment? World J Mens Health

;38:254-5.

Isidori AM, Giannetta E, Giannetta, Pofi R, Venneri MA,

Gianfrilli D, Campolo F, et al. Targeting the NO‐cGMP‐PDE5

pathway in COVID‐19 infection Andrology. 2020:10.1111/

andr.12837.

Chowdhury B, Luu AZ, Luu VZ, Kabir MG, Pan Y, Teoh H,

et al. The SGLT2 inhibitor empagliflozin reduces mortality and

prevents progression in experimental pulmonary hypertension.

Biochem Biophys Res Commun 2020;524:50-6.

Aroor AR, Das NA, Carpenter AJ, Habibi J, Jia G,

Ramirez Perez FI, et al. Glycemic control by the SGLT2

inhibitor empagliflozin decreases aortic stiffness, renal resistive

index and kidney injury. Cardiovasc Diabetol 2018;17:108.

Zhang Q, Ju Y, Ma Y, Wang T. N acetylcysteine improves

oxidative stress and inflammatory response in patients with

community acquired pneumonia. A randomized controlled trial.

Medicine (Baltimore) 2018;97:e13087.