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The Molecular Mechanisms Involved in Axonal Degeneration and Retrograde Retinal Ganglion Cell Death
Zhaoyang Zuo1, Ziyuan Zhang1, Siming Zhang1
1Department of Ophthalmology, Second Hospital of Jilin University, Changchun, China.
Abstract:
Axonal degeneration is a pathologic change common to multiple retinopathies and optic neuropathies. Various pathologic factors, such as mechanical injury, inflammation, and ischemia, can damage retinal ganglion cell (RGC) somas and axons, eventually triggering axonal degeneration and RGC death. The molecular mechanisms of somal and axonal degeneration are distinct but also overlap, and axonal degeneration can result in retrograde somal degeneration. While the mitogen-activated protein kinase pathway acts as a central node in RGC axon degeneration, several newly discovered molecules, such as sterile alpha and Toll/interleukin-1 receptor motif-containing protein 1 and nicotinamide mononucleotide adenylyltransferase 2, also play a critical role in this pathological process following different types of injury. Therefore, we summarize the types of injury that cause RGC axon degeneration and retrograde RGC death and important underlying molecular mechanisms, providing a reference for the identification of targets for protecting axons and RGCs.
Insights
Retinal ganglion cell (RGC) axon degeneration, common in optic neuropathies, is triggered by various injuries. New molecular targets are emerging for protecting RGC axons and cell bodies.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Axonal degeneration is a key pathological feature in various retinopathies and optic neuropathies.
- Damage to retinal ganglion cell (RGC) somas and axons can result from mechanical injury, inflammation, or ischemia.
- Both axonal and somal degeneration share distinct yet overlapping molecular mechanisms, with axonal damage potentially leading to retrograde somal degeneration.
Purpose of the Study:
- To review the types of injuries that induce RGC axon degeneration and retrograde RGC death.
- To summarize the critical molecular mechanisms underlying these degenerative processes.
- To provide a reference for identifying therapeutic targets for RGC axon and cell body protection.
Main Methods:
- Literature review of studies on RGC axon degeneration and optic neuropathies.
- Analysis of molecular pathways involved in RGC injury and survival.
- Synthesis of information on injury types and their associated molecular mechanisms.
Main Results:
- Identified mechanical injury, inflammation, and ischemia as common causes of RGC axon degeneration.
- Highlighted the central role of the mitogen-activated protein kinase pathway in RGC axon degeneration.
- Introduced newly discovered molecules, including sterile alpha and Toll/interleukin-1 receptor motif-containing protein 1 and nicotinamide mononucleotide adenylyltransferase 2, as critical players in RGC degeneration following injury.
Conclusions:
- Understanding the distinct and overlapping molecular mechanisms of axonal and somal degeneration is crucial.
- Specific molecular players and pathways offer potential targets for neuroprotection in retinopathies and optic neuropathies.
- Further research into these mechanisms can guide the development of strategies to preserve vision by protecting RGCs.
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