Literature DB >> 33342421

Possible therapeutic interventions in COVID-19 induced ARDS by cotinine as an ACE-2 promoter and AT-1R blocker.

Tarun Sharma1, Sidharth Mehan1.   

Abstract

In these challenging times of the pandemic, as coronavirus disease 2019 (COVID-19) has taken over the planet, its complications such as acute respiratory distress syndrome (ARDS) have the potential to wipe out a large portion of our population. Whereas a serious lack of ventilators, vaccine being months away makes the condition even worse. That's why promising drug therapy is required. One of them was suggested in this article. It is the angiotensin-converting enzyme-2 (ACE-2) to which the COVID-19 virus binds and upon downregulation of which the pulmonary permeability increases and results in the filling of alveoli by proteinaceous fluids, which finally results in ARDS. ARDS can be assisted by angiotensinII type-1 receptor (AT-1R) blocker and ACE-2 upregulator. AT-1R blocker will prevent vasoconstriction, the proinflammatory effect seen otherwise upon its activation. ACE-2 upregulation will ensure less formation of angiotensin II, vasodilatory effects due to the formation of angiotensin (1-7), increased breakdown of bradykinin at lung level. Overall, decreased vasoconstriction of vessels supplying lungs and decreased vasodilation of lung tissues will ensure decreased pulmonary permeability and eventually relieve ARDS. It should also be considered that all components of the reninangiotensin-aldosterone system (RAAS) are located in the lung tissues. A drug with the least plasma protein binding is required to ensure its distribution across these lung tissues. Cotinine appears to be a promising candidate for COVID-19- induced ARDS. It acts across the board and acts as both an AT-1R blocker, ACE-2 upregulator. It also has a weak plasma protein binding that helps to spread through the lung tissues. In this review, we summarized that cotinine, along with COVID-19 virus replication blocker anti-virals, may prove to be a promising therapy for the treatment of COVID-19 induced ARDS. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.

Entities:  

Keywords:  Coronavirus disease 2019 (COVID19); acute respiratory distress syndrome (ARDS); angiotensin-II; angiotensin-II type-1 receptor (AT-1R); angiotensin-converting enzyme-2 (ACE-2); rennin angiotensinzzm321990aldosterone system (RAAS)

Year:  2020        PMID: 33342421     DOI: 10.2174/1871526520666201218153554

Source DB:  PubMed          Journal:  Infect Disord Drug Targets        ISSN: 1871-5265


  2 in total

1.  Molecular Effects of Auto-Antibodies on Angiotensin II Type 1 Receptor Signaling and Cell Proliferation.

Authors:  Aurélie Philippe; Gunnar Kleinau; Jason Jannis Gruner; Sumin Wu; Daniel Postpieszala; David Speck; Harald Heidecke; Simon J Dowell; Gabriela Riemekasten; Peter W Hildebrand; Julian Kamhieh-Milz; Rusan Catar; Michal Szczepek; Duska Dragun; Patrick Scheerer
Journal:  Int J Mol Sci       Date:  2022-04-02       Impact factor: 5.923

Review 2.  Angiotensin and Endothelin Receptor Structures With Implications for Signaling Regulation and Pharmacological Targeting.

Authors:  David Speck; Gunnar Kleinau; Michal Szczepek; Dennis Kwiatkowski; Rusan Catar; Aurélie Philippe; Patrick Scheerer
Journal:  Front Endocrinol (Lausanne)       Date:  2022-04-19       Impact factor: 6.055

  2 in total

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