Oxidative Stress and the Neurovascular Unit

Rinaldi, Carmela; Donato, Luigi; Alibrandi, Simona; Scimone, Concetta; D’Angelo, Rosalia; Sidoti, Antonina

doi:10.3390/life11080767

Cited by 49 publications

(42 citation statements)

References 196 publications

(218 reference statements)

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“…Systemic, endocrine, neural factor, and oxidative stress disorders of the neurovascular unit (NVU) can contribute to the development of a brain injury, and play a major role in dysregulation, neuroinflammation, and neurodegeneration after a stroke. Complex communication and cell-to-cell communication is essential [ 10 , 11 ]; for example, pericyte modulators, such as the NADPH oxidase Nox4 (reactive oxygen species (ROS)), are significantly increased under hypoxic conditions, increasing MMP-9 and possibly increasing the size of the infarct area by playing a harmful role in the acute phase of ischemic stroke [ 11 ].…”

Section: Discussionmentioning

confidence: 99%

Non-Simultaneous Bilateral Ischemic Optic Neuropathy Related to High Altitude and Airplane Flight in a Patient with Cerebral Small Vessel Disease

et al. 2021

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Non-arteritic anterior ischemic optic neuropathy (NA-AION) is considered the most frequent type of acute optic neuropathy. A 61-year-old woman presented with a NA-AION in her right eye within 24 h following an airplane flight. One year later, after driving for 10 days with a daily accumulated altitude of 1500 m, she developed a NA-AION in her left eye. Systemic disorders were investigated, and cerebral small vessel disease was observed via cranial computed tomography. An inadequate response to hypoxia, in a patient with individual susceptibility, could lead to reduced blood supply to the optic nerve head, which could represent an underlying cause of NA-AION.

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Section: Discussionmentioning

confidence: 99%

Non-Simultaneous Bilateral Ischemic Optic Neuropathy Related to High Altitude and Airplane Flight in a Patient with Cerebral Small Vessel Disease

et al. 2021

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“…Chronic hyperglycemia can be a trigger for the impairment of neurovascular units via intracellular excess glucose flux followed by overproduction of reactive oxygen species (ROS) and advanced glycation-end products (AGEs) [51]. AGEs can be sources for ROS production and ROS is associated with mitochondrial dysfunction, resulting in the disturbance of the blood barrier function and the impairment of neuronal tissue homeostasis [52]. However, it was recently reported that microglia to be members of the neurovascular unit.…”

Section: Pathogenesis Of the Diabetic Retinopathy: The Impairment Of The Neurovascular Unitmentioning

confidence: 99%

“…Oxidative stress including overproduction of ROS results in ER stress related cell death or pyroptosis (Figure 3) and noncoding RNAs are involved in alteration of ROS homeostasis induced by oxidative stress [52]. Oxidative stress induces the alteration of several transcription factors such as AP-1, p53, or NF-κB which are involved in immune response, growth factor signaling, and neurodegeneration [52]. These possible involvements of epigenetic mechanisms induced by oxidative stress are also important, but go beyond the scope of this review.…”

Section: Mechanisms Of Neuronal Cell Death In Rgc Neuropathy In Diabetic Retinamentioning

confidence: 99%

The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina

Oshitari

2021

IJMS

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Diabetic retinopathy is a major retinal disease and a leading cause of blindness in the world. Diabetic retinopathy is a neurovascular disease that is associated with disturbances of the interdependent relationship of cells composed of the neurovascular units, i.e., neurons, glial cells, and vascular cells. An impairment of these neurovascular units causes both neuronal and vascular abnormalities in diabetic retinopathy. More specifically, neuronal abnormalities including neuronal cell death and axon degeneration are irreversible changes that are directly related to the vision reduction in diabetic patients. Thus, establishment of neuroprotective and regenerative therapies for diabetic neuropathy in the retina is an emergent task for preventing the blindness of patients with diabetic retinopathy. This review focuses on the pathogenesis of the neuronal abnormalities in diabetic retina including glial abnormalities, neuronal cell death, and axon degeneration. The possible molecular cell death pathways and intrinsic survival and regenerative pathways are also described. In addition, therapeutic approaches for diabetic neuropathy in the retina both in vitro and in vivo are presented. This review should be helpful for providing clues to overcome the barriers for establishing neuroprotection and regeneration of diabetic neuropathy in the retina.

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“…In the diabetic retina, the interdependence between different cell types consisting of the NVUs is impeded by many stresses, including the polyol pathway [ 36 ], the hexosamine pathway [ 37 ], oxidative stress [ 38 , 39 ], protein kinase C (PKC) [ 40 , 41 ], advanced glycation-end products (AGEs) [ 42 ], and inflammation [ 43 ]. The hypothetic scheme of the neurovascular impairments provoked by these stresses in diabetic retinopathy is shown in Figure 1 .…”

Section: Physiology and Pathology Of Nvu In Diabetic Retinopathymentioning

confidence: 99%

Neurovascular Impairment and Therapeutic Strategies in Diabetic Retinopathy

Oshitari

2021

IJERPH

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Diabetic retinopathy has recently been defined as a highly specific neurovascular complication of diabetes. The chronic progression of the impairment of the interdependence of neurovascular units (NVUs) is associated with the pathogenesis of diabetic retinopathy. The NVUs consist of neurons, glial cells, and vascular cells, and the interdependent relationships between these cells are disturbed under diabetic conditions. Clinicians should understand and update the current knowledge of the neurovascular impairments in diabetic retinopathy. Above all, neuronal cell death is an irreversible change, and it is directly related to vision loss in patients with diabetic retinopathy. Thus, neuroprotective and vasoprotective therapies for diabetic retinopathy must be established. Understanding the physiological and pathological interdependence of the NVUs is helpful in establishing neuroprotective and vasoprotective therapies for diabetic retinopathy. This review focuses on the pathogenesis of the neurovascular impairments and introduces possible neurovascular protective therapies for diabetic retinopathy.

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Oxidative Stress and the Neurovascular Unit

Cited by 49 publications

References 196 publications

Non-Simultaneous Bilateral Ischemic Optic Neuropathy Related to High Altitude and Airplane Flight in a Patient with Cerebral Small Vessel Disease

Non-Simultaneous Bilateral Ischemic Optic Neuropathy Related to High Altitude and Airplane Flight in a Patient with Cerebral Small Vessel Disease

The Pathogenesis and Therapeutic Approaches of Diabetic Neuropathy in the Retina

Neurovascular Impairment and Therapeutic Strategies in Diabetic Retinopathy

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