ReviewClinical and experimental medicine2023
Modulation of IRAK enzymes as a therapeutic strategy against SARS-CoV-2 induced cytokine storm.
Review in Clinical and experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Time-Resolved Transcriptomic Profiling of Chandipura Virus Infection Reveals Dynamic Host Responses and Host-Directed Therapeutic Targets.International journal of molecular sciences · 2026Article
- Acute Hyperglycaemia, Insulin Resistance, and Cytokine Dysregulation as Predictors of Disease Severity in Non-Diabetic Hospitalised COVID-19 Patients.International journal of molecular sciences · 2026Article
- Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response.Frontiers in aging · 2026Review
- Phosphoregulation of interleukin-1 receptor-associated kinase 1 in inflammatory signaling.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of the current pandemic coronavirus disease 2019 (COVID-19). Dysregulated and excessive production of cytokines and chemokines, known as cytokine storm, is frequently seen in patients with severe COVID-19 disease and it can provoke a severe systematic inflammation in the patients. The IL-1R/TLRs/IRAKs signaling network is a key pathway in immune cells that plays a central role in regulating innate immunity and inflammatory responses via stimulating the expression and production of various proinflammatory molecules including cytokines. Modulation of IRAKs activity has been proposed to be a promising strategy in the treatment of inflammatory disorders. In this review, we highlight the biochemical properties of IRAKs and their role in regulating inflammatory molecular signaling pathways and discuss the potential targeting of IRAKs to suppress the SARS-CoV-2-induced cytokine storm in COVID-19 patients.
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