Tissue injury in nonmalignant human disease can develop from either disproportionate inflammation or exaggerated fibrotic responses. The molecular and cellular fundamental of these 2 processes, their impact on disease prognosis and the treatment concept deviates fundamentally. Consequently, the synchronous assessment and quantification of these 2 processes in vivo is extremely desirable. Although noninvasive molecular techniques such as F-fluorodeoxyglucose PET offer insights into the degree of inflammatory activity, the assessment of the molecular dynamics of fibrosis remains challenging. The Ga-fibroblast activation protein inhibitor-46 may improve noninvasive clinical diagnostic performance in patients with both fibroinflammatory pathology and long-term CT-abnormalities after severe COVID-19.
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http://dx.doi.org/10.1016/j.cpet.2023.02.004 | DOI Listing |
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