ArticleEMBO molecular medicine2022
CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.
Article in EMBO molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
16 citing papers in PubMed, 20 citations in OpenAlex.
- Prognosis of Right Ventricular Systolic Dysfunction in Patients With Duchenne Muscular Dystrophy.Journal of the American Heart Association · 2023Trial
- Beta-nicotinamide mononucleotide attenuates creatine kinase release in Duchenne muscular dystrophy model rats.The Journal of veterinary medical science · 2026Article
- CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.Molecular neurobiology · 2025Review
- Cardiac intermediary metabolism in heart failure: substrate use, signalling roles and therapeutic targets.Nature reviews. Cardiology · 2025Review
- Emerging strategies, applications and challenges of targeting NADNature aging · 2025Review
- The role of NADnpj metabolic health and disease · 2025Review
- Article
- Immunoregulation in cancer-associated cachexia.Journal of advanced research · 2024Review
- Retention of stress susceptibility in the mdx mouse model of Duchenne muscular dystrophy after PGC-1α overexpression or ablation of IDO1 or CD38.Human molecular genetics · 2024Article
- NAD metabolism: Role in senescence regulation and aging.Aging cell · 2024Review
- Review
- Transcriptomic analysis of paired healthy human skeletal muscles to identify modulators of disease severity in DMD.Frontiers in genetics · 2023Article
- Role of Liver CD38 in the Regulation of Metabolic Pathways during Cold-Induced Thermogenesis in Mice.Cells · 2022Article
- Diaphragm muscle function in a mouse model of early-onset spasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- CD38-NADase is a new major contributor to Duchenne muscular dystrophic phenotype.EMBO molecular medicine · 2022Article
- Brain derived neurotrophic factor/tropomyosin related kinase B signaling impacts diaphragm neuromuscular transmission in a novel rat chemogenetic model.Frontiers in cellular neuroscience · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
25 authors at 4 institutions in 2 countries.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is characterized by progressive muscle degeneration. Two important deleterious features are a Ca
Indexed as
Identifiers
What OpenQuestion holds
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.