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Targeting SARS-CoV-2-Induced Cardiovascular Injury: Exploring the Potential of Ponatinib in Mitigating Cardiovascular
Mohammad Javad Sotoudeheian1, Reza Azarbad2, Seyed-Mohamad-Sadegh Mirahmadi3,4
1Physiology Research Center, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Insights
Coronavirus Disease 2019 (COVID-19) can cause heart damage through various mechanisms, including direct viral interaction with ACE-2 receptors. This study explores ponatinib as a potential therapy to mitigate COVID-19-related cardiotoxicity by targeting cell death pathways.
Area of Science:
- Cardiology
- Virology
- Pharmacology
Background:
- Coronavirus Disease 2019 (COVID-19) significantly impacts global health, with cardiovascular complications posing a major threat.
- SARS-CoV-2 entry via angiotensin-converting enzyme 2 (ACE-2) receptors can lead to direct myocardial damage.
- Mechanisms of COVID-19-induced heart injury include inflammation, fibrosis, and necroptosis.
Purpose of the Study:
- To review the mechanisms of cardiomyocyte injury in COVID-19.
- To investigate the potential of ponatinib in reducing COVID-19-related cardiotoxicity.
- To propose novel therapeutic strategies for cardiac protection during COVID-19.
Main Methods:
- Literature review of COVID-19's cardiovascular effects.
- Analysis of SARS-CoV-2 interaction with ACE-2 receptors.
- Exploration of ponatinib's mechanism of action on cell death pathways, particularly necroptosis.
Main Results:
- COVID-19 can induce myocardial damage through multiple pathways, with necroptosis being a key mechanism.
- Ponatinib, a tyrosine kinase inhibitor, shows potential in modulating cell death processes.
- Current treatments for cardiac damage include IL-6 blockers and antiplatelet therapy.
Conclusions:
- Understanding COVID-19's impact on the cardiovascular system is crucial.
- Ponatinib presents a promising therapeutic avenue for mitigating COVID-19-induced cardiotoxicity.
- Further research is essential to develop targeted treatments for cardiac protection against COVID-19.
Abstract:
The incidence of Coronavirus Disease 2019 (COVID-19) has increased dramatically in recent years, affecting millions of people worldwide. The primary cause of morbidity and mortality in COVID-19 patients is respiratory illness. However, the disease can also significantly impact the cardiovascular system. SARS-CoV-2, the virus responsible for COVID-19, enters cells using the angiotensin-converting enzyme 2 (ACE-2) receptor. ACE-2 is a component of the renin-angiotensin system (RAS) and plays a crucial role in regulating various pathological processes. The interaction of the virus with ACE-2 in the myocardium can lead to direct heart damage. Several mechanisms may contribute to myocardial damage in COVID-19 patients, including systemic inflammation, myocardial interstitial fibrosis, interferon-mediated immune response, exaggerated cytokine response, T-cell-mediated damage, coronary plaque instability, and hypoxia. There has been concern that ACE inhibitors (ACE-Is) and angiotensin receptor blockers (ARBs) may increase vulnerability to SARS-CoV-2 by upregulating ACE-2 expression. However, it may be advisable to continue medications for patients with underlying cardiovascular disorders. The precise mechanisms of cardiomyocyte injury in COVID-19 are not fully understood, but necroptosis appears to play a significant role. Current treatments for cardiac damage in COVID-19 patients include IL-6 blockers and antiplatelet therapy. Ponatinib, a small molecule tyrosine kinase inhibitor designed using computational and structural approaches, has shown the potential to affect cell death through its impact on tyrosine kinase activity. By reviewing studies related to ponatinib's effects on necroptosis and cell death, we propose a novel approach to potentially reduce the cardiotoxic effects of COVID-19 on cardiomyocytes. Further research is needed to fully elucidate the mechanisms of cardiac injury in COVID-19 and to develop targeted therapies to protect the heart from the devastating effects of this disease.
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