ReviewMolecular neurobiology2025
CD38-NAD(+) Axis: New Insights into Glaucoma Therapy.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- The Eye as a Window to Neurodegeneration: Oxidative Stress, Optic Nerve Vulnerability, and Retinal Biomarkers-A Scoping Review.Antioxidants (Basel, Switzerland) · 2026Review
- Low-Dose Ionizing Radiation and Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Review of Recent Evidence and Future Research Directions Toward the Elucidation of a Metabolic, Immunologic, and Signaling Cascade.International journal of molecular sciences · 2026Review
- Review
- Stage- and compartment-specific remodeling of autophagy and selective mitophagy in glaucoma: from aqueous outflow dysfunction to retinal ganglion cell neurodegeneration.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Glaucoma is a globally recognized leading cause of irreversible blindness, and its progression is closely associated with retinal ganglion cell (RGC) degeneration and mitochondrial dysfunction. Recently, there has been growing interest in the role of nicotinamide adenine dinucleotide (NAD +) and its regulatory enzyme CD38 in the pathogenesis and progression of glaucoma. NAD + plays a critical role in cellular energy metabolism and signal transduction, and its depletion is strongly linked to mitochondrial dysfunction and neurodegenerative diseases. The function of CD38 in glaucoma primarily involves modulating oxidative stress, inflammatory responses, and apoptosis by regulating NAD + levels. With advancing age, the expression of CD38 tends to increase, leading to reduced NAD + levels. Studies have demonstrated that inhibition or absence of CD38 can elevate NAD + levels, thereby enhancing the activity of NAD + -dependent enzymes (such as Sirt1) to protect RGCs from injury and mitigate retinal ischemia-reperfusion injury and inflammation. Furthermore, animal studies have indicated that supplementation with NAD + precursors (such as nicotinamide) can delay glaucoma progression by restoring the neuroprotective effects mediated by NAD + . This review systematically examines the interplay between NAD + and CD38 in glaucoma pathogenesis and explores potential therapeutic strategies targeting the CD38/NAD + axis. Despite promising experimental findings supporting this approach, current research still faces challenges such as drug selectivity, side effects, and validation of treatment efficacy. Future investigations into optic neuroprotection in glaucoma should focus on elucidating the precise mechanisms of the CD38/NAD + axis within retinal tissue to develop more effective glaucoma therapies.
Indexed as
Identifiers
40696206What Socratic 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 Socratic graph.