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TL;DR
The authors synthesize laboratory findings indicating that in AMD, excessive reactive oxygen species (ROS) production may promote mitophagy in the RPE via the p62/Nrf2 pathway.
Cellular and Molecular Neurobiology · 5 authors, 1 centre
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The authors synthesize laboratory findings indicating that in AMD, excessive reactive oxygen species (ROS) production may promote mitophagy in the RPE via the p62/Nrf2 pathway.
The authors synthesize laboratory findings indicating that in AMD, excessive reactive oxygen species (ROS) production may promote mitophagy in the RPE via the p62/Nrf2 pathway. It proposes that regulating mitophagy could be a novel therapeutic strategy but notes significant challenges, including the complexity of interacting signaling pathways and the lack of highly efficient, specific drugs.