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@ARTICLE{Scholz:269672,
author = {Scholz, Rebekka and Brösamle, Desirée and Yuan, Xidi and
Beyer, Marc and Neher, Jonas J},
title = {{E}pigenetic control of microglial immune responses.},
journal = {Immunological reviews},
volume = {323},
number = {1},
issn = {0105-2896},
address = {Oxford},
publisher = {Wiley-Blackwell},
reportid = {DZNE-2024-00586},
pages = {209 - 226},
year = {2024},
abstract = {Microglia, the major population of brain-resident
macrophages, are now recognized as a heterogeneous
population comprising several cell subtypes with different
(so far mostly supposed) functions in health and disease. A
number of studies have performed molecular characterization
of these different microglial activation states over the
last years making use of 'omics' technologies, that is
transcriptomics, proteomics and, less frequently,
epigenomics profiling. These approaches offer the
possibility to identify disease mechanisms, discover novel
diagnostic biomarkers, and develop new therapeutic
strategies. Here, we focus on epigenetic profiling as a
means to understand microglial immune responses beyond what
other omics methods can offer, that is, revealing past and
present molecular responses, gene regulatory networks and
potential future response trajectories, and defining cell
subtype-specific disease relevance through mapping
non-coding genetic variants. We review the current knowledge
in the field regarding epigenetic regulation of microglial
identity and function, provide an exemplary analysis that
demonstrates the advantages of performing joint
transcriptomic and epigenomic profiling of single microglial
cells and discuss how comprehensive epigenetic analyses may
enhance our understanding of microglial pathophysiology.},
subtyp = {Review Article},
keywords = {Microglia: immunology / Microglia: metabolism / Epigenesis,
Genetic / Humans / Animals / Epigenomics: methods /
Transcriptome / Immunity: genetics / Gene Regulatory
Networks / Gene Expression Profiling / Brain: immunology /
Brain: metabolism / ATAC‐seq (Other) / ATAC‐seq (Other)
/ Alzheimer (Other) / ChIP‐seq (Other) / aging (Other) /
epigenetics (Other) / microglia (Other) / ChIP‐seq
(Other)},
cin = {AG Neher (Tübingen) / AG Beyer / PRECISE},
ddc = {610},
cid = {I:(DE-2719)1210012 / I:(DE-2719)1013035 /
I:(DE-2719)1013031},
pnm = {352 - Disease Mechanisms (POF4-352) / 351 - Brain Function
(POF4-351)},
pid = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-351},
experiment = {EXP:(DE-2719)PRECISE-20190321},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:38491845},
doi = {10.1111/imr.13317},
url = {https://pub.dzne.de/record/269672},
}