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2014 ; 53
(ä): 33-43
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General pathophysiology in retinal degeneration
#MMPMID24732759
Wert KJ
; Lin JH
; Tsang SH
Dev Ophthalmol
2014[]; 53
(ä): 33-43
PMID24732759
show ga
Retinal degeneration, including that seen in age-related macular degeneration and
retinitis pigmentosa (RP), is the most common form of neural degenerative disease
in the world. There is great genetic and allelic heterogeneity of the various
retinal dystrophies. Classifications of these diseases can be ambiguous, as there
are similar clinical presentations in retinal degenerations arising from
different genetic mechanisms. As would be expected, alterations in the activity
of the phototransduction cascade, such as changes affecting the renewal and
shedding of the photoreceptor OS, visual transduction, and/or retinol metabolism
have a great impact on the health of the retina. Mutations within any of the
molecules responsible for these visual processes cause several types of retinal
and retinal pigment epithelium degenerative diseases. Apoptosis has been
implicated in the rod cell loss seen in a mouse model of RP, but the precise
mechanisms that connect the activation of these pathways to the loss of
phosphodiesterase (PDE6?) function has yet to be defined. Additionally, the
activation of apoptosis by CCAAT/-enhancer-binding protein homologous protein
(CHOP), after activation of the unfolded protein response pathway, may be
responsible for cell death, although the mechanism remains unknown. However, the
mechanisms of cell death after loss of function of PDE6, which is a commonly
studied mammalian model in research, may be generalizable to loss of function of
different key proteins involved in the phototransduction cascade.
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