ArticleJACC. Basic to translational science2025
Low-Grade Inflammation in Long COVID Syndrome Sustains a Persistent Platelet Activation Associated With Lung Impairment.
Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Tissue-specific autoantibody signatures reveal immune alterations undetected by routine serology in long COVID.GeroScience · 2026Article
- Clinical relevance of circulating blood microaggregates and reactivation of Epstein Barr Virus in long-term Post-CoVID syndrome patients.Scientific reports · 2026Article
- Platelet Autophagy as a Druggable Intracellular Pathway: Therapeutic Opportunities in Thromboinflammatory Diseases.Pharmaceutics · 2026Review
- Interpretable machine learning for predicting low-dose methylprednisolone effectiveness in long COVID.iScience · 2026Article
- Insulin Resistance and Inflammation.International journal of molecular sciences · 2026Review
- Platelet-derived mediators in hospitalized COVID-19 patients and associations to respiratory failure, ICU admittance and 60-day mortality.Frontiers in cardiovascular medicine · 2026Article
- Principal component analysis of cytokine signature in COVID-19 and Long COVID.Frontiers in immunology · 2026Article
- P-Selectin and Platelet-Monocyte Interaction in Inflammation: Mechanisms, Hypothesis, and Open Questions.Journal of inflammation research · 2026Review
- Article
- Dysregulated monocyte compartment in PACS patients.Frontiers in immunology · 2025Article
- The Lung and Winding Road: Inflammation-Driven Platelet Reactivity in Long COVID.JACC. Basic to translational science · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the present study, we provide evidence on the potential mechanisms involved in the residual pulmonary impairment described in long COVID syndrome. Data highlight that lung damage is significantly associated with a proinflammatory platelet phenotype, characterized mainly by the formation of platelet-leukocyte aggregates. In ex vivo experiments, long COVID plasma reproduces the platelet activation observed in vivo and highlights low-grade inflammation as a potential underpinning mechanism, exploiting a synergistic activity between C-reactive protein and subthreshold concentrations of interleukin-6. The platelet-activated phenotype is blunted by anti-inflammatory and antiplatelet drugs, suggesting a potential therapeutic option in this clinical setting.
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