ReviewInflammopharmacology2021
Neuropathophysiology of coronavirus disease 2019: neuroinflammation and blood brain barrier disruption are critical pathophysiological processes that contribute to the clinical symptoms of SARS-CoV-2 infection.
Review in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.
- Pooled it
- Unraveling the cardiovascular burden of long COVID: symptom profiles, underlying mechanisms, and clinical management insights.Frontiers in cardiovascular medicine · 2026Review
- COVID-19 and female reproductive health: pathophysiological mechanisms and clinical reproductive outcomes.Frontiers in medicine · 2026Review
- Post-COVID Condition and Neuroinflammation: Possible Management with Antioxidants.Antioxidants (Basel, Switzerland) · 2025Review
- Review
- COVID-19 and cognitive impairment: a review of the emerging evidence.Discover mental health · 2025Review
- Innate immune sensors and regulators at the blood brain barrier: focus on toll-like receptors and inflammasomes as mediators of neuro-immune crosstalk and inflammation.Journal of neuroinflammation · 2025Review
- Decreases in frequency-dependent intrinsic activity of the default mode network are associated with depression and cognition in patients with postacute sequelae of SARS-CoV-2 infection.Brain structure & function · 2025Article
- New-onset refractory status epilepticus after SARS-CoV-2 infection: a review of literature.Croatian medical journal · 2024Review
- Neurological complications caused by SARS-CoV-2.Clinical microbiology reviews · 2024Review
- The Role of ACE2 in Neurological Disorders: From Underlying Mechanisms to the Neurological Impact of COVID-19.International journal of molecular sciences · 2024Review
- Article
- Neurological sequelae of long COVID: a comprehensive review of diagnostic imaging, underlying mechanisms, and potential therapeutics.Frontiers in neurology · 2024Review
- Clinical and immunological features in patients with neuroimmune complications of COVID-19 during Omicron wave in China: a case series.Frontiers in immunology · 2024Article
- Sudden Hearing Loss Waves: The Effect of COVID-19 Infection and Vaccination on the Inner Ear.Advances in experimental medicine and biology · 2024Review
- The Hidden Impact of Covid-19 on Memory: Disclosing Subjective Complaints.Clinical neuropsychiatry · 2023Article
- Recombinant SARS-CoV-2 Spike Protein and Its Receptor Binding Domain Stimulate Release of Different Pro-Inflammatory Mediators via Activation of Distinct Receptors on Human Microglia Cells.Molecular neurobiology · 2023Article
- Quantum Dot Biomimetic for SARS-CoV-2 to Interrogate Blood-Brain Barrier Damage Relevant to NeuroCOVID Brain Inflammation.ACS applied nano materials · 2023Article
- Long COVID, the Brain, Nerves, and Cognitive Function.Neurology international · 2023Review
- Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy.Pharmaceutics · 2023Review
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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Coronavirus disease 2019 (COVID-19) is caused by the novel SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) first discovered in Wuhan, Hubei province, China in December 2019. SARS-CoV-2 has infected several millions of people, resulting in a huge socioeconomic cost and over 2.5 million deaths worldwide. Though the pathogenesis of COVID-19 is not fully understood, data have consistently shown that SARS-CoV-2 mainly affects the respiratory and gastrointestinal tracts. Nevertheless, accumulating evidence has implicated the central nervous system in the pathogenesis of SARS-CoV-2 infection. Unfortunately, however, the mechanisms of SARS-CoV-2 induced impairment of the central nervous system are not completely known. Here, we review the literature on possible neuropathogenic mechanisms of SARS-CoV-2 induced cerebral damage. The results suggest that downregulation of angiotensin converting enzyme 2 (ACE2) with increased activity of the transmembrane protease serine 2 (TMPRSS2) and cathepsin L in SARS-CoV-2 neuroinvasion may result in upregulation of proinflammatory mediators and reactive species that trigger neuroinflammatory response and blood brain barrier disruption. Furthermore, dysregulation of hormone and neurotransmitter signalling may constitute a fundamental mechanism involved in the neuropathogenic sequelae of SARS-CoV-2 infection. The viral RNA or antigenic peptides also activate or interact with molecular signalling pathways mediated by pattern recognition receptors (e.g., toll-like receptors), nuclear factor kappa B, Janus kinase/signal transducer and activator of transcription, complement cascades, and cell suicide molecules. Potential molecular targets and therapeutics of SARS-CoV-2 induced neurologic damage are also discussed.
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Registered trials
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