Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19

Al-Kuraishy, Hayder M; Al-Gareeb, Ali I; Mostafa‐Hedeab, Gomaa; Kasozi, Keneth Iceland; Zirintunda, Gerald; Aslam, Akhmed; Allahyani, Mamdouh; Welburn, Susan C.; Batiha, Gaber El‐Saber

doi:10.3389/fimmu.2021.749291

Cited by 51 publications

(47 citation statements)

References 114 publications

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“…In its clinical perspective, IVN might be a pioneer drug in attenuating cardiotoxicity, mainly in patients with heart failure, arrhythmias, and malignancies treated by DXR. It has been shown that unlike β-blockers, IVN does not decrease ventricular force (Su et al 2020 ; Al-Kuraishy et al 2021b , 2022c , d ; Lawal et al 2021 ) and can also reduce COVID-19-induced cardiovascular complications due to its anti-inflammatory and antioxidant properties (Al-Kuraishy et al 2021c , 2022e ; Batiha et al 2021 , 2022 ). In addition, IVN facilitates a pleiotropic cardioprotective effect against isoproterenol-induced acute cardiac injury by increasing the ventricular fibrillation threshold (Simko et al 2021 ).…”

Section: Discussionmentioning

confidence: 99%

The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument

et al. 2022

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This study investigated the potential role of ivabradine (IVN) in the attenuation of doxorubicin (DXR)-induced cardiotoxicity in rats. A total of 28 Swiss-Albino male mice were used, divided into four equal groups: the negative control did not receive any agents ( n = 7), the DXR group received a single dose of DXR 20 mg/kg ( n = 7), the treated group A was pretreated with IVN 5 mg/kg plus DXR ( n = 7), and the treated group B was pretreated with IVN 10 mg/kg plus DXR ( n = 7). The duration of this study was 10 days. Inflammatory biomarkers, including tumor necrosis factor alpha (TNF-α), lactate dehydrogenase (LDH), malondialdehyde (MDA), and cardiac troponin (cTn-I) serum levels were measured. TNF-α, LDH, MDA, and cTn-I serum levels were higher in the DXR-treated mice compared with the control ( P ˂0.01). IVN produced a dose-dependent effect in the reduction of MDA and cTn-I compared to DXR-treated mice ( P ˂0.05). Our findings suggest that IVN is an effective agent in mitigating DXR-induced cardiotoxicity due to its anti-inflammatory and antioxidant effects. IVN illustrated a dose-dependent effect in the attenuation of DXR-induced cardiotoxicity through inhibition of lipid peroxidation and cardiomyocyte injury.

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Section: Discussionmentioning

confidence: 99%

The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument

et al. 2022

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“…Notably, oxidative stress is linked with the progression of SARS-CoV-2 infection and COVID-19 severity due to ROS generation, mitochondrial dysfunction, dysregulation of RAS, and reduction of endogenous antioxidant capacity (Cecchini and Cecchini 2020 ). In turn, oxidative stress triggers release of pro-inflammatory cytokines via activation of inflammatory signaling pathways including nuclear factor kappa B (NF-κB), nod-like receptor pyrin 3 receptor (NLRP3) inflammasome and p38 mitogen activated protein kinase (p38MAPK) (Al-Kuraishy et al 2022a ; Mostafa-Hedeab et al 2022 ; Al-Kuraishy et al 2021g ). Pro-inflammatory cytokines and activated inflammatory signaling pathways interacted together in the induction of oxidative stress in SARS-CoV-2 infection (Al-Kuraishy et al 2022b ).…”

Section: Citicoline Oxidative Stress and Hyperinflammationmentioning

confidence: 99%

Citicoline and COVID-19: vis-à-vis conjectured

Al-Kuraishy

Al-Buhadily

Al-Gareeb

et al. 2022

Naunyn-Schmiedeberg's Arch Pharmacol

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Coronavirus disease 2019 (COVID-19) is a current pandemic disease caused by a novel severe acute respiratory syndrome coronavirus virus respiratory type 2 (SARS-CoV-2). SARS-CoV-2 infection is linked with various neurological manifestations due to cytokine-induced disruption of the blood brain barrier (BBB), neuroinflammation, and peripheral neuronal injury, or due to direct SARS-CoV-2 neurotropism. Of note, many repurposed agents were included in different therapeutic protocols in the management of COVID-19. These agents did not produce an effective therapeutic eradication of SARS-CoV-2, and continuing searching for novel anti-SARS-CoV-2 agents is a type of challenge nowadays. Therefore, this study aimed to review the potential anti-inflammatory and antioxidant effects of citicoline in the management of COVID-19.

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“…A retrospective analysis demonstrated that the use of alpha-1 adrenergic receptor antagonists reduced COVID-19 in-hospital mortality by 77% (odds ratio (OR): 0.23; 95% CI: 0.03-0.94; p = 0.028) [ 56 ], while beta-blockers reduced the inflammatory response that led to cytokine storms in COVID-19 [ 57 ]. In addition, SARS-CoV-2 mRNA vaccination has been followed by multiple cases of Takotsubo cardiomyopathy [ 58 ], a syndrome triggered by excessive catecholamine release and activity [ 59 ].…”

Section: Reviewmentioning

confidence: 99%

Catecholamines Are the Key Trigger of COVID-19 mRNA Vaccine-Induced Myocarditis: A Compelling Hypothesis Supported by Epidemiological, Anatomopathological, Molecular, and Physiological Findings

Cadegiani¹

2022

Cureus

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mRNA vaccine-induced myocarditis is a rare but well-documented complication in young males. The increased incidence of sudden death among athletes following vaccination has been reported and requires further investigation. Whether the risk of myocarditis, a known major cause of sudden death in young male athletes, also increases after coronavirus disease 2019 (COVID-19) infection is unknown. The severity and implications of these critical adverse effects require a thorough analysis to elucidate their key triggering mechanisms. The present review aimed to evaluate whether there is a justification to hypothesize that catecholamines in a “hypercatecholaminergic” state are the key trigger of SARS-CoV-2 mRNA vaccine-induced myocarditis and related outcomes and whether similar risks are also present following COVID-19 infection. A thorough, structured scoping review of the literature was performed to build the hypothesis through three pillars: detection of myocarditis risk, potential alterations and abnormalities identified after SARS-CoV-2 mRNA vaccination or COVID-19 infection and consequent events, and physiological characteristics of the most affected population. The following terms were searched in indexed and non-indexed peer review articles and recent preprints (<12 months): agent, “SARS-CoV-2” or “COVID-19”; event, “myocarditis” or “sudden death(s)” or “myocarditis+sudden death(s)” or “cardiac event(s)”; underlying cause, “mRNA” or “spike protein” or “infection” or “vaccine”; proposed trigger, “catecholamine(s)” or “adrenaline” or “epinephrine” or “noradrenaline” or “norepinephrine” or “testosterone”; and affected population, “young male(s)” or “athlete(s).” The rationale and data that supported the hypothesis were as follows: SARS-CoV-2 mRNA vaccine-induced myocarditis primarily affected young males, while the risk was not observed following COVID-19 infection; independent autopsies or biopsies of patients who presented post-SARS-CoV-2 mRNA vaccine myocarditis in different geographical regions enabled the conclusion that a primary hypercatecholaminergic state was the key trigger of these events; SARS-CoV-2 mRNA was densely present, and SARS-CoV-2 spike protein was progressively produced in adrenal medulla chromaffin cells, which are responsible for catecholamine production; the dihydroxyphenylalanine decarboxylase enzyme that converts dopamine into noradrenaline was overexpressed in the presence of SARS-CoV-2 mRNA, leading to enhanced noradrenaline activity; catecholamine responses were physiologically higher in young adults and males than in other populations; catecholamine responses and resting catecholamine production were higher in male athletes than in non-athletes; catecholamine responses to stress and its sensitivity were enhanced in the presence of androgens; and catecholamine expressions in young male athletes were already high at baseline, were higher following vaccination, and were higher than those in non-vaccinated athle...

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Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19

Cited by 51 publications

References 114 publications

The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument

The role of ivabradine in doxorubicin-induced cardiotoxicity: exploring of underlying argument

Citicoline and COVID-19: vis-à-vis conjectured

Catecholamines Are the Key Trigger of COVID-19 mRNA Vaccine-Induced Myocarditis: A Compelling Hypothesis Supported by Epidemiological, Anatomopathological, Molecular, and Physiological Findings

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