ReviewBioscience reports2020
Immunotherapy of COVID-19 with poly (ADP-ribose) polymerase inhibitors: starting with nicotinamide.
Review in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Targeted inhibition of PARP-1 in pulmonary epithelial cells and macrophages via SPA-functionalized microparticles attenuates sepsis-induced lung injury.Materials today. Bio · 2026Article
- Post-booster longitudinal plasma proteomic changes following BNT162b2 COVID-19 vaccination in Qatar.Frontiers in immunology · 2026Article
- NAD+ metabolism and therapeutic strategies in cardiovascular diseases.Atherosclerosis plus · 2024Review
- The Biology and Biochemistry of Kynurenic Acid, a Potential Nutraceutical with Multiple Biological Effects.International journal of molecular sciences · 2024Review
- A glimpse into viral warfare: decoding the intriguing role of highly pathogenic coronavirus proteins in apoptosis regulation.Journal of biomedical science · 2024Review
- Potential association between COVID-19 and neurological disorders: analysis of common genes and therapeutics.Frontiers in neurology · 2024Article
- The kynurenine pathway of tryptophan metabolism: a neglected therapeutic target of COVID-19 pathophysiology and immunotherapy.Bioscience reports · 2023Article
- Repurposing and computational design of PARP inhibitors as SARS-CoV-2 inhibitors.Scientific reports · 2023Article
- SARS-CoV-2 infection dysregulates NAD metabolism.Frontiers in immunology · 2023Article
- [Research Progress in Niacinamide in the Prevention and Treatment of Mouth and Systemic Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Review
- Tryptophan metabolism and disposition in cancer biology and immunotherapy.Bioscience reports · 2022Article
- Tryptophan Metabolism 'Hub' Gene Expression Associates with Increased Inflammation and Severe Disease Outcomes in COVID-19 Infection and Inflammatory Bowel Disease.International journal of molecular sciences · 2022Article
- Nicotinamide pathways as the root cause of sepsis - an evolutionary perspective on macrophage energetic shifts.The FEBS journal · 2022Review
- Species Differences in Tryptophan Metabolism and Disposition.International journal of tryptophan research : IJTR · 2022Review
- Therapeutic Potential of Emerging NAD+-Increasing Strategies for Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- CD38 in the age of COVID-19: a medical perspective.Physiological reviews · 2021Review
- Therapeutic Significance of microRNA-Mediated Regulation of PARP-1 in SARS-CoV-2 Infection.Non-coding RNA · 2021Article
- Multiple roles of haem in cystathionine β-synthase activity: implications for hemin and other therapies of acute hepatic porphyria.Bioscience reports · 2021Article
- ACE2-lentiviral transduction enables mouse SARS-CoV-2 infection and mapping of receptor interactions.PLoS pathogens · 2021Article
- [Aryl hydrocarbon receptor modulates airway inflammation in mice with cockroach allergen-induced asthma by regulating Th17/Treg differentiation].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
COVID-19 induces a proinflammatory environment that is stronger in patients requiring intensive care. The cytokine components of this environment may determine efficacy or otherwise of glucocorticoid therapy. The immunity modulators, the aryl hydrocarbon receptor (AhR) and the nuclear NAD+-consuming enzyme poly (ADP-ribose) polymerase 1 (PARP 1) may play a critical role in COVID-19 pathophysiology. The AhR is overexpressed in coronaviruses, including COVID-19 and, as it regulates PARP gene expression, the latter is likely to be activated in COVID-19. PARP 1 activation leads to cell death mainly by depletion of NAD+ and adenosine triphosphate (ATP), especially when availability of these energy mediators is compromised. PARP expression is enhanced in other lung conditions: the pneumovirus respiratory syncytial virus (RSV) and chronic obstructive pulmonary disease (COPD). I propose that PARP 1 activation is the terminal point in a sequence of events culminating in patient mortality and should be the focus of COVID-19 immunotherapy. Potent PARP 1 inhibitors are undergoing trials in cancer, but a readily available inhibitor, nicotinamide (NAM), which possesses a highly desirable biochemical and activity profile, merits exploration. It conserves NAD+ and prevents ATP depletion by PARP 1 and Sirtuin 1 (silent mating type information regulation 2 homologue 1) inhibition, enhances NAD+ synthesis, and hence that of NADP+ which is a stronger PARP inhibitor, reverses lung injury caused by ischaemia/reperfusion, inhibits proinflammatory cytokines and is effective against HIV infection. These properties qualify NAM for therapeutic use initially in conjunction with standard clinical care or combined with other agents, and subsequently as an adjunct to stronger PARP 1 inhibitors or other drugs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.