Cardiovascular protective properties of oxytocin against COVID-19
Stephani C Wang1, Yu-Feng Wang2
1Division of Cardiology, Department of Medicine, University of California-Irvine, Irvine, CA, USA.
Insights
Oxytocin (OXT) may treat and prevent COVID-19 by protecting the heart and vasculature. This neuropeptide suppresses inflammation and viral invasion, offering a safe alternative to other treatments.
Area of Science:
- Cardiovascular Medicine
- Immunology
- Neuropeptide Research
Background:
- COVID-19 causes significant cardiovascular morbidity and mortality, with effective treatments still needed.
- Cardiovascular complications are key drivers of severe COVID-19 outcomes.
- New therapeutic strategies targeting cardiovascular aspects are crucial for disease management.
Purpose of the Study:
- To explore the potential of oxytocin (OXT) in managing COVID-19-associated cardiovascular complications.
- To summarize the cardiovascular pathogenesis of COVID-19.
- To discuss the challenges and therapeutic applications of OXT in COVID-19.
Main Methods:
- Review of current literature on COVID-19 cardiovascular pathology.
- Analysis of OXT's proposed mechanisms of action against SARS-CoV-2.
- Evaluation of OXT's safety and efficacy compared to existing treatments.
Main Results:
- OXT demonstrates immune-regulating functions, suppressing inflammation and cytokine storm.
- OXT can inhibit viral entry by affecting enzymes like cathepsin L and TMPRSS2.
- OXT protects the heart and vasculature by reducing hypertension and promoting cardiomyocyte regeneration.
Conclusions:
- OXT presents a promising therapeutic candidate for COVID-19, particularly for cardiovascular complications.
- OXT's safety profile appears favorable compared to remdesivir and corticosteroids.
- Further research is needed to fully establish OXT's role in COVID-19 treatment and prevention.
Abstract:
SARS-CoV-2 infection or COVID-19 has become a worldwide pandemic; however, effective treatment for COVID-19 remains to be established. Along with acute respiratory distress syndrome (ARDS), new and old cardiovascular injuries are important causes of significant morbidity and mortality in COVID-19. Exploring new approaches managing cardiovascular complications is essential in controlling the disease progression and preventing long-term complications. Oxytocin (OXT), an immune-regulating neuropeptide, has recently emerged as a strong candidate for treatment and prevention of COVID-19 pandemic. OXT carries special functions in immunologic defense, homeostasis and surveillance. It suppresses neutrophil infiltration and inflammatory cytokine release, activates T-lymphocytes, and antagonizes negative effects of angiotensin II and other key pathological events of COVID-19. Additionally, OXT can promote γ-interferon expression to inhibit cathepsin L and increases superoxide dismutase expression to reduce heparin and heparan sulphate fragmentation. Through these mechanisms, OXT can block viral invasion, suppress cytokine storm, reverse lymphocytopenia, and prevent progression to ARDS and multiple organ failures. Importantly, besides prevention of metabolic disorders associated with atherosclerosis and diabetes mellitus, OXT can protect the heart and vasculature through suppressing hypertension and brain-heart syndrome, and promoting regeneration of injured cardiomyocytes. Unlike other therapeutic agents, exogenous OXT can be used safely without the side-effects seen in remdesivir and corticosteroid. Importantly, OXT can be mobilized endogenously to prevent pathogenesis of COVID-19. This article summarizes our current understandings of cardiovascular pathogenesis caused by COVID-19, explores the protective potentials of OXT against COVID-19-associated cardiovascular diseases, and discusses challenges in applying OXT in treatment and prevention of COVID-19. CHEMICAL COMPOUNDS: Angiotensin-converting enzyme 2 (ACE2); atrial natriuretic peptide (ANP); cathepsin L; heparan sulphate proteoglycans (HSPGs); interferon; interleukin; oxytocin; superoxide dismutase; transmembrane serine protease isoform 2 (TMPRSS2).
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