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@ARTICLE{Ilyinsky:1028212,
author = {Ilyinsky, Nikolay S. and Nesterov, Semen V. and
Shestoperova, Elizaveta I. and Fonin, Alexander V. and
Uversky, Vladimir N. and Gordeliy, Valentin I.},
title = {{O}n the {R}ole of {N}ormal {A}ging {P}rocesses in the
{O}nset and {P}athogenesis of {D}iseases {A}ssociated with
the {A}bnormal {A}ccumulation of {P}rotein {A}ggregates},
journal = {Biochemistry (Moscow)},
volume = {86},
number = {3},
issn = {0006-2979},
address = {Dordrecht [u.a.]},
publisher = {Springer Science + Business Media B.V},
reportid = {FZJ-2024-04406},
pages = {275 - 289},
year = {2021},
abstract = {Aging is a prime systemic cause of various age-related
diseases, in particular, proteinopathies. In fact, most
diseases associated with protein misfolding are sporadic,
and their incidence increases with aging. This review
examines the process of protein aggregate formation, the
toxicity of such aggregates, the organization of cellular
systems involved in proteostasis, and the impact of protein
aggregates on important cellular processes leading to
proteinopathies. We also analyze how manifestations of aging
(mitochondrial dysfunction, dysfunction of signaling
systems, changes in the genome and epigenome) facilitate
pathogenesis of various proteinopathies either directly, by
increasing the propensity of key proteins for aggregation,
or indirectly, through dysregulation of stress responses.
Such analysis might help in outlining approaches for
treating proteinopathies and extending healthy longevity.},
cin = {IBI-7},
ddc = {540},
cid = {I:(DE-Juel1)IBI-7-20200312},
pnm = {5241 - Molecular Information Processing in Cellular Systems
(POF4-524)},
pid = {G:(DE-HGF)POF4-5241},
typ = {PUB:(DE-HGF)16},
pubmed = {33838629},
UT = {WOS:000629221900003},
doi = {10.1134/S0006297921030056},
url = {https://juser.fz-juelich.de/record/1028212},
}