ReviewFrontiers in immunology2021
Effects of β-Blockers on the Sympathetic and Cytokines Storms in Covid-19.
Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
36 citing papers in PubMed, 64 citations in OpenAlex.
- A brain-lung circuit drives LPS-induced lung injury via sympathetic neutrophil axis.Journal of neuroinflammation · 2026Article
- Rewiring the Lung-CNS Axis After Spinal Cord Injury.Journal of inflammation research · 2026Review
- The potential role of carvedilol in COVID-19 management: perspective and take-away.Inflammopharmacology · 2025Review
- A Transformer-Based Framework for Counterfactual Estimation of Antihypertensive Treatment Effect on COVID-19 Infection Risk - A Proof-of-Concept Study.American journal of hypertension · 2025Article
- Adrenergic blockers, statins, and non-steroidal anti-inflammatory drugs are associated with later age at onset in Parkinson's disease.Journal of neurology · 2025Article
- Decrypting the Possible Mechanistic Role of Fenofibrate in Alzheimer's Disease and Type 2 Diabetes: The Truth and Mystery.Journal of cellular and molecular medicine · 2025Review
- Interleukin-6 related signaling pathways as the intersection between chronic diseases and sepsis.Molecular medicine (Cambridge, Mass.) · 2025Review
- The Effects of Beta-Blockers on Leukocytes and the Leukocyte Subpopulation in Heart Failure Patients.Biomedicines · 2024Article
- Neurological complications caused by SARS-CoV-2.Clinical microbiology reviews · 2024Review
- β-blockers and metabolic modulation: unraveling the complex interplay with glucose metabolism, inflammation and oxidative stress.Frontiers in pharmacology · 2024Review
- The possible role furin and furin inhibitors in endometrial adenocarcinoma: A narrative review.Cancer reports (Hoboken, N.J.) · 2024Review
- Interplay of TLR4 and SARS-CoV-2: Unveiling the Complex Mechanisms of Inflammation and Severity in COVID-19 Infections.Journal of inflammation research · 2024Review
- Dysmenorrhea severity in war refugees with hypertension: a cross-talk with antihypertensives and analgesics.African health sciences · 2023Article
- New insights on the potential effect of progesterone in Covid-19: Anti-inflammatory and immunosuppressive effects.Immunity, inflammation and disease · 2023Review
- SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway.Cell stress & chaperones · 2023Review
- Evolution of Cardiovascular Risk Factors in Post-COVID Patients.Journal of clinical medicine · 2023Article
- Does colchicine reduce mortality in patients with COVID-19 clinical syndrome? An umbrella review of published meta-analyses.Heliyon · 2023Review
- Antidepressants and type 2 diabetes: highways to knowns and unknowns.Diabetology & metabolic syndrome · 2023Review
- Relative Bradycardia and Tachycardia and Their Associations with Adverse Outcomes in Hospitalized COVID-19 Patients.Reviews in cardiovascular medicine · 2023Article
- Review
Corrections and comments
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Authors and funding
9 authors at 8 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a causative virus in the development of coronavirus disease 2019 (Covid-19) pandemic. Respiratory manifestations of SARS-CoV-2 infection such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) leads to hypoxia, oxidative stress, and sympatho-activation and in severe cases leads to sympathetic storm (SS). On the other hand, an exaggerated immune response to the SARS-CoV-2 invasion may lead to uncontrolled release of pro-inflammatory cytokine development of cytokine storm (CS). In Covid-19, there are interactive interactions between CS and SS in the development of multi-organ failure (MOF). Interestingly, cutting the bridge between CS and SS by anti-inflammatory and anti-adrenergic agents may mitigate complications that are induced by SARS-CoV-2 infection in severely affected Covid-19 patients. The potential mechanisms of SS in Covid-19 are through different pathways such as hypoxia, which activate the central sympathetic center through carotid bodies chemosensory input and induced pro-inflammatory cytokines, which cross the blood-brain barrier and activation of the sympathetic center. β2-receptors signaling pathway play a crucial role in the production of pro-inflammatory cytokines, macrophage activation, and B-cells for the production of antibodies with inflammation exacerbation. β-blockers have anti-inflammatory effects through reduction release of pro-inflammatory cytokines with inhibition of NF-κB. In conclusion, β-blockers interrupt this interaction through inhibition of several mediators of CS and SS with prevention development of neural-cytokine loop in SARS-CoV-2 infection. Evidence from this study triggers an idea for future prospective studies to confirm the potential role of β-blockers in the management of Covid-19.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.