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.
Song et al. (Sat,) studied this question.