Abstract
p62/sequestosome-1 is a multidimensional protein that interacts with many signaling factors, and regulates a variety of cellular functions including inflammation, apoptosis, and autophagy. Our previous work has revealed in the retinal pigment epithelium (RPE) that p62 promotes autophagy and simultaneously enhances an Nrf2-mediated antioxidant response to protect against acute oxidative stress. Several recent studies demonstrated that p62 contributes to NFkB mediated inflammation and inflammasome activation under certain circumstances, raising the question of whether p62 protects against or contributes to tissue injury. Herein, we will review the general characteristics of p62, focusing on its pro- and anti-cell survival roles within different physiological/pathological contexts, and discuss the potential of p62 as a therapeutic target for AMD.
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Acknowledgments
Funding for this work was provided by NIH EY019904 (JTH), Beckman Foundation AMD Grant (JTH), Thome Foundation (JTH), Research to Prevent Blindness Senior Scientist Award (JTH), NIH P30EY001765 core grant, the Robert Bond Welch Professorship (JTH), a gift from the Merlau family, and an unrestricted grant from RPB to the Wilmer Eye Institute.
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Wang, L., Ebrahimi, K., Chyn, M., Cano, M., Handa, J. (2016). Biology of p62/sequestosome-1 in Age-Related Macular Degeneration (AMD). In: Bowes Rickman, C., LaVail, M., Anderson, R., Grimm, C., Hollyfield, J., Ash, J. (eds) Retinal Degenerative Diseases. Advances in Experimental Medicine and Biology, vol 854. Springer, Cham. https://doi.org/10.1007/978-3-319-17121-0_3
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DOI: https://doi.org/10.1007/978-3-319-17121-0_3
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