Photoreceptor metabolic reprogramming: current understanding and therapeutic implications.
Photoreceptor metabolic reprogramming: current understanding and therapeutic implications.
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DOI:
10.1038/s42003-021-01765-3
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发表时间:
2021-02-24
影响因子:
5.9
通讯作者:
Besirli CG
中科院分区:
文献类型:
--
作者:
Pan WW;Wubben TJ;Besirli CG
Acquired and inherited retinal disorders are responsible for vision loss in an increasing proportion of individuals worldwide. Photoreceptor (PR) death is central to the vision loss individuals experience in these various retinal diseases. Unfortunately, there is a lack of treatment options to prevent PR loss, so an urgent unmet need exists for therapies that improve PR survival and ultimately, vision. The retina is one of the most energy demanding tissues in the body, and this is driven in large part by the metabolic needs of PRs. Recent studies suggest that disruption of nutrient availability and regulation of cell metabolism may be a unifying mechanism in PR death. Understanding retinal cell metabolism and how it is altered in disease has been identified as a priority area of research. The focus of this review is on the recent advances in the understanding of PR metabolism and how it is critical to reduction-oxidation (redox) balance, the outer retinal metabolic ecosystem, and retinal disease. The importance of these metabolic processes is just beginning to be realized and unraveling the metabolic and redox pathways integral to PR health may identify novel targets for neuroprotective strategies that prevent blindness in the heterogenous group of retinal disorders. Photoreceptor death is central to vision loss in various retinal diseases. Disruption of nutrient availability and cell metabolism may underlie photoreceptor death. In this review, Pan et al. focus on the recent advances in the understanding of photoreceptor metabolism and suggest novel targets for neuroprotective strategies that prevent blindness.
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DOI:
10.1186/2046-2395-3-6
发表时间:
2014
期刊:
Longevity & healthspan
影响因子:
--
作者:
Dai DF;Chiao YA;Marcinek DJ;Szeto HH;Rabinovitch PS
通讯作者:
Rabinovitch PS
影响因子:
3.5
作者:
Bryan, John M.;Fufa, Temesgen D.;McGaughey, David M.
通讯作者:
McGaughey, David M.
影响因子:
5.5
作者:
Daniele, Lauren L.;Sauer, Brian;Philp, Nancy J.
通讯作者:
Philp, Nancy J.
影响因子:
14.8
作者:
Anastasiou, Dimitrios;Yu, Yimin;Israelsen, William J.;Jiang, Jian-Kang;Boxer, Matthew B.;Hong, Bum Soo;Tempel, Wolfram;Dimov, Svetoslav;Shen, Min;Jha, Abhishek;Yang, Hua;Mattaini, Katherine R.;Metallo, Christian M.;Fiske, Brian P.;Courtney, Kevin D.;Malstrom, Scott;Khan, Tahsin M.;Kung, Charles;Skoumbourdis, Amanda P.;Veith, Henrike;Southall, Noel;Walsh, Martin J.;Brimacombe, Kyle R.;Leister, William;Lunt, Sophia Y.;Johnson, Zachary R.;Yen, Katharine E.;Kunii, Kaiko;Davidson, Shawn M.;Christofk, Heather R.;Austin, Christopher P.;Inglese, James;Harris, Marian H.;Asara, John M.;Stephanopoulos, Gregory;Salituro, Francesco G.;Jin, Shengfang;Dang, Lenny;Auld, Douglas S.;Park, Hee-Won;Cantley, Lewis C.;Thomas, Craig J.;Heiden, Matthew G. Vander
通讯作者:
Heiden, Matthew G. Vander
影响因子:
4.4
作者:
Curcio CA
通讯作者:
Curcio CA