bims-mideyd Biomed News
on Mitochondrial dysfunction in eye diseases
Issue of 2026–03–01
two papers selected by
Rajalekshmy “Raji” Shyam, University of Iowa
  1. Mitochondrial Resilience in Glaucoma: Targeting NAD+ Metabolism and Oxidative Stress in Retinal Ganglion Cell Degeneration with Nicotinamide Riboside and Berberine: Preliminary Clinical Evidence.
  2. Exercise-Induced Irisin: A Novel Strategy for Neuroinflammation Alleviation and Neurorepair in Diabetic Retinopathy.
  1. Diseases. 2026 Feb 02. pii: 56. [Epub ahead of print]14(2):
    Mitochondrial Resilience in Glaucoma: Targeting NAD+ Metabolism and Oxidative Stress in Retinal Ganglion Cell Degeneration with Nicotinamide Riboside and Berberine: Preliminary Clinical Evidence.
    Federico Visalli, Francesco Cappellani, Giuseppe Gagliano, Alfonso Spinello, Alessandro Avitabile, Ludovica Cannizzaro, Matteo Capobianco, Caterina Gagliano, Marco Zeppieri.
       BACKGROUND: Glaucoma is a chronic neurodegenerative disorder characterized by the selective vulnerability of retinal ganglion cells (RGCs), in which mitochondrial dysfunction, redox imbalance, and impaired bioenergetic signaling play central pathogenetic roles. Mitochondrial homeostasis in RGCs critically depends on maintaining intracellular NAD+ pools, which support oxidative phosphorylation, sirtuin-mediated deacetylation, and antioxidant gene expression. Nicotinamide riboside (NR), a potent NAD+ precursor, and berberine (BBR), an AMPK activator derived from Berberis aristata, have recently emerged as synergistic modulators of mitochondrial metabolism and oxidative stress resistance.
    METHODS: This study retrospectively assessed clinical outcomes associated with combined nutraceutical supplementation of nicotinamide riboside (NR) and berberine (BBR) in patients with primary open-angle glaucoma undergoing stable topical hypotensive therapy. We have included a narrative review in the current literature regarding NAD+ biology, AMPK-sirtuin signaling, and oxidative stress responses in retinal ganglion cell (RGC) degeneration. Due to the absence of comparator groups receiving only NR or only berberine in this retrospective cohort, the combined supplementation has been regarded as a biologically complementary strategy, and the potential for synergistic efficacy remains a subject for further investigation.
    RESULTS: Translationally, a retrospective clinical cohort receiving combined NR and BBR supplementation showed functional stabilization of the visual field and structural preservation of the retinal nerve fiber layer over a six-month follow-up, in line with the proposed mitochondrial protective mechanisms.
    CONCLUSIONS: The clinical trends identified in this retrospective cohort have substantiated the translational significance of NR + BBR supplementation as a potential adjunctive approach in glaucoma management. NAD+ repletion and engagement of the AMPK-SIRT-NRF2 pathway may enhance mitochondrial resilience in RGCs. Collectively, these findings offer initial clinical evidence advocating for additional controlled studies on NR + berberine supplementation, while mechanistic interpretations have been derived from the existing literature and are hypothesis-generating.
    Keywords:  NAD+ metabolism; berberine; glaucoma; mitochondrial dysfunction; neuroprotection; nicotinamide; nicotinamide riboside; oxidative stress; retinal ganglion cells
    DOI:  https://doi.org/10.3390/diseases14020056
  2. Int J Mol Sci. 2026 Feb 14. pii: 1849. [Epub ahead of print]27(4):
    Exercise-Induced Irisin: A Novel Strategy for Neuroinflammation Alleviation and Neurorepair in Diabetic Retinopathy.
    Hanlai Song, Yuxian Jiang, Shun Zhang, Chenmian Wu, Chaohua Deng, Weikun Hu.
      Diabetic retinopathy (DR) stands as a classic microvascular complication of diabetes mellitus. DR is characterized by multidimensional pathological changes in retinal neurons, microvasculature and supportive cells, leading to an intricate damage network. It is predominantly marked by neuropathy, encompassing retinal neuronal dysfunction, aberrant activation of glial cells, and degeneration of synaptic structures. In severe instances, it can result in visual impairment and, in the worst-case scenario, blindness. As diabetes progresses, retinal nerve tissue frequently sustains damage owing to oxidative stress, inflammatory responses, and compromised mitochondrial function. Although the precise neuroprotective mechanisms remain elusive, exercise has the ability to bolster mitochondrial function in retinal cells, diminish oxidative stress, and curb inflammatory reactions, thereby safeguarding the neurophysiological function of the retina. Irisin is a myokine primarily secreted by skeletal muscles in response to exercise stimulation. Moreover, being produced in trace amounts across a variety of tissues, it has the capacity to regulate the physiological processes of multiple organs. Recent studies have indicated that irisin can exert powerful neuroprotective effects by enhancing cellular glucose uptake, improving mitochondrial function, inhibiting the expression of pro-inflammatory factors, and resisting ferroptosis. In this review, we systematically collated and synthesized existing evidence on irisin-related signaling pathways and comprehensively assessed its regulatory potential in alleviating neuroinflammation and promoting neural repair in diabetic retinopathy and offer insights into future research directions in this field.
    Keywords:  diabetic retinopathy; ferroptosis; inflammation; irisin; neuroprotection; physical exercise
    DOI:  https://doi.org/10.3390/ijms27041849
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