Vasoactive Peptides: Role in COVID-19 Pathogenesis and Potential Use as Biomarkers and Therapeutic Targets.

BACKGROUND: The ongoing outbreak of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), as the latest threat to global health, causes overwhelming effects for the public healthcare systems worldwide. Of note, in addition to the respiratory complications, some patients with coronavirus disease 2019 (COVID-19) also develop serious cardiovascular injuries. Vasoactive peptides play an important role in a wide range of physiological and pathological conditions. AIM: With the urgent need for exploring the specific therapeutic targets and biomarkers for the emerging COVID-19, the general aim of this review is to discuss the potentials of the vasoactive peptides including Angiotensin II (Ang II), vasoactive intestinal peptide (VIP), endothelin-1 (ET-1), calcitonin gene-related peptide (CGRP), natriuretic peptides, substance P (SP) and bradykinin (BK) as therapeutic targets and/or prognostic indicators for the COVID-19 pandemic. CONCLUSION: Based on various observations some authors conclude that the assessment of vasoactive peptides shall be considered a routine part of COVID-19 patient monitoring, and they can serve as potential therapeutic targets for the disease management.

Therapeutic Status of Famotidine in COVID-19 Patients: A Review.

The novel coronavirus, SARS-coV-2, which emerged in Wuhan in November 2019, has increasingly spread worldwide. More than 272 million cases of infection have been identified. COVID-19 has affected 223 countries and territories across the world. The principal target of the SARS-CoV-2 infection is the lower respiratory tract. Series of moderate to non-specific severe clinical signs and symptoms appear two to fourteen days after exposure to SARS-CoV-2 in patients with COVID-19 disease, including cough, breath deficiency, and at least two of these symptoms: headache, fever, chills, repeated rigor, myalgia, oropharyngitis, anosmia, and ageusia. No therapeutic agents have been validated to have substantial efficacy in the clinical care of COVID-19 patients in large-scale trials, despite worsening infected rates of COVID-19. Early clinical evidence from many sources suggests that treatment with famotidine may decrease COVID-19-related morbidity and mortality. The mechanism by which famotidine could improve the outcomes of COVID-19 is currently unknown. A more recent postulated mechanism is that the effect of famotidine is mediated by histamine-2 receptor antagonism or inverse agonism, inferring that the SARS-CoV-2, resulting in COVID-19 infection, at least partially leads to the abnormal release of histamine and perhaps dysfunction of mast cells.