ArticleBMB reports2022
Hyper-inflammatory responses in COVID-19 and anti-inflammatory therapeutic approaches.
Article in BMB reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 6 citations in OpenAlex.
- The controversial interplay between hyperinflammation and immunosenescence in elderly critically ill co-infected patients.BMC geriatrics · 2026Article
- Discovery of synthetic G-quadruplex DNA as SARS-CoV-2 helicase inhibitor with antiviral, anti-inflammatory and antioxidative properties.Cell death discovery · 2026Article
- Cognition, Cytokines, Blood-Brain Barrier, and Beyond in COVID-19: A Narrative Review.International journal of molecular sciences · 2026Review
- Safety and efficacy of selective RIPK1 inhibitor SIR1-365 in hospitalized patients with severe COVID-19: A multicenter, randomized, double-blind, phase 1b trial.Journal of intensive medicine · 2025Article
- SARS-CoV2 is not just infection but a culprit of donor graft failure post-allogeneic stem cell transplant.Clinical hematology international · 2024Article
- Anti-SARS-CoV-2 Activity ofMolecules (Basel, Switzerland) · 2023Article
- Establishment of the large-scale longitudinal multi-omics dataset in COVID-19 patients: data profile and biospecimen.BMB reports · 2022Article
- NRF2 activation by 2-methoxycinnamaldehyde attenuates inflammatory responses in macrophages via enhancing autophagy flux.BMB reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The coronavirus disease 2019 (COVID-19) is an ongoing global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Patients with severe COVID-19 exhibit hyper-inflammatory responses characterized by excessive activation of myeloid cells, including monocytes, macrophages, and neutrophils, and a plethora of pro-inflammatory cytokines and chemokines. Accumulating evidence also indicates that hyperinflammation is a driving factor for severe progression of the disease, which has prompted the development of anti-inflammatory therapies for the treatment of patients with COVID-19. Corticosteroids, IL-6R inhibitors, and JAK inhibitors have demonstrated promising results in treating patients with severe disease. In addition, diverse forms of exosomes that exert anti-inflammatory functions have been tested experimentally for the treatment of COVID-19. Here, we briefly describe the immunological mechanisms of the hyper-inflammatory responses in patients with severe COVID-19. We also summarize current anti-inflammatory therapies for the treatment of severe COVID-19 and novel exosome-based therapeutics that are in experimental stages. [BMB Reports 2022; 55(1): 11-19].
Indexed as
Identifiers
34903319PMC8810550W4200628685What OpenQuestion holds
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.