Microcirculation (New York, N.Y. : 1994) · 2026
Microvascular Dysfunction and Redox Imbalance in Long COVID.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Lewandowska Adela, Sawicka Dominika, Jóźwiak Aleksandra, Jędrzejewska Agata, Braczko Alicja, Romanowska-Kocejko Marzena, Żarczyńska-Buchowiecka Marta, Kutryb-Zając Barbara, Hellmann Marcin, Mierzejewska Paulina
Аннотация
OBJECTIVE: Endothelial and microvascular dysfunction are key features of Long COVID. Disturbances in cellular redox balance, reflected by altered nicotinamide adenine dinucleotide (NAD+/NADH) dynamics, may underlie vascular impairment. Flow-Mediated Skin Fluorescence (FMSF) evaluates microvascular function by monitoring NADH fluorescence during ischemia and reperfusion. We integrated FMSF-derived microvascular phenotyping with targeted NAD+ metabolite profiling to determine whether altered NAD+ metabolism is associated with impaired microvascular responses in Long COVID.
METHODS: Microvascular function was assessed in 36 patients with Long COVID and 47 age-matched controls using FMSF. NADH fluorescence changes during ischemia and hyperemia were analyzed as markers of endothelial responsiveness. NAD+ and related metabolites were measured using high-performance liquid chromatography and mass spectrometry.
RESULTS: Patients with Long COVID showed impaired FMSF parameters, including blunted ischemic responses and delayed recovery after hyperemia, indicating microvascular dysfunction. These changes were accompanied by a reduced NAD+/NADH ratio and lower NADP levels, consistent with redox imbalance. Abnormal fluorescence profiles were associated with altered NAD+ metabolism, including reduced precursor availability and accumulation of degradation products. Higher NR concentrations showed associations with selected microvascular and eNOS-related parameters.
CONCLUSIONS: FMSF provides a clinically applicable tool for detecting microvascular dysfunction in Long COVID. NAD+ redox imbalance is linked to impaired microcirculatory responses, supporting FMSF as a functional marker of microvascular impairment associated with altered NAD+ metabolism.
METHODS: Microvascular function was assessed in 36 patients with Long COVID and 47 age-matched controls using FMSF. NADH fluorescence changes during ischemia and hyperemia were analyzed as markers of endothelial responsiveness. NAD+ and related metabolites were measured using high-performance liquid chromatography and mass spectrometry.
RESULTS: Patients with Long COVID showed impaired FMSF parameters, including blunted ischemic responses and delayed recovery after hyperemia, indicating microvascular dysfunction. These changes were accompanied by a reduced NAD+/NADH ratio and lower NADP levels, consistent with redox imbalance. Abnormal fluorescence profiles were associated with altered NAD+ metabolism, including reduced precursor availability and accumulation of degradation products. Higher NR concentrations showed associations with selected microvascular and eNOS-related parameters.
CONCLUSIONS: FMSF provides a clinically applicable tool for detecting microvascular dysfunction in Long COVID. NAD+ redox imbalance is linked to impaired microcirculatory responses, supporting FMSF as a functional marker of microvascular impairment associated with altered NAD+ metabolism.