ArticleClinical pathology (Thousand Oaks, Ventura County, Calif.)
Rationale for Nicotinamide Adenine Dinucleotide (NAD+) Metabolome Disruption as a Pathogenic Mechanism of Post-Acute COVID-19 Syndrome.
Article in Clinical pathology (Thousand Oaks, Ventura County, Calif.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 19 citations in OpenAlex.
- NADThe Journal of general virology · 2026Review
- Differential Factors Associated With the Presence of Persistent Symptoms in Individuals Diagnosed With Long COVID: Protocol for a Longitudinal Matched Case-Control Study.JMIR research protocols · 2026Observational
- Vitamin D and Mitochondrial Activity Preservation in COVID-19.Infectious disorders drug targets · 2025Article
- Dysregulated nicotinamide adenine dinucleotide metabolome in patients hospitalized with COVID-19.Aging cell · 2024Article
- Post-Acute Sequelae and Mitochondrial Aberration in SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
- Article
- Mitochondria in COVID-19: from cellular and molecular perspective.Frontiers in physiology · 2024Review
- [Acid-base balance and long COVID: comments on metabolic-respiratory alterations].Revista de la Facultad de Ciencias Medicas (Cordoba, Argentina) · 2023Article
- Gut Microbiota and Mitochondria: Health and Pathophysiological Aspects of Long COVID.International journal of molecular sciences · 2023Review
- PARPs and ADP-Ribosylation in Chronic Inflammation: A Focus on Macrophages.Pathogens (Basel, Switzerland) · 2023Review
- ME/CFS and Long COVID share similar symptoms and biological abnormalities: road map to the literature.Frontiers in medicine · 2023Review
- Editor-in-Chief's Commentary:Sage open pathologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Many acute COVID-19 convalescents experience a persistent sequelae of infection, called post-acute COVID-19 syndrome (PACS). With incidence ranging between 31% and 69%, PACS is becoming increasingly acknowledged as a new disease state in the context of SARS-CoV-2 infection. As SARS-CoV-2 infection can affect several organ systems to varying degrees and durations, the cellular and molecular abnormalities contributing to PACS pathogenesis remain unclear. Despite our limited understanding of how SARS-CoV-2 infection promotes this persistent disease state, mitochondrial dysfunction has been increasingly recognized as a contributing factor to acute SARS-CoV-2 infection and, more recently, to PACS pathogenesis. The biological mechanisms contributing to this phenomena have not been well established in previous literature; however, in this review, we summarize the evidence that NAD+ metabolome disruption and subsequent mitochondrial dysfunction following SARS-CoV-2 genome integration may contribute to PACS biological pathogenesis. We also briefly examine the coordinated and complex relationship between increased oxidative stress, inflammation, and mitochondrial dysfunction and speculate as to how SARS-CoV-2-mediated NAD+ depletion may be causing these abnormalities in PACS. As such, we present evidence supporting the therapeutic potential of intravenous administration of NAD+ as a novel treatment intervention for PACS symptom management.
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