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MicroRNA-146a is a wide-reaching neuroinflammatory regulator and potential treatment target in neurological diseases

Fan, Weihao, Liang, Chunmei, Ou, Mingqian, Zou, Ting, Sun, Furong, Zhou, Haihong, Cui, Lili·2020·Frontiers in Molecular Neuroscience
DOI 10.3389/fnmol.2020.00090PMC PMC7291868
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  • The miR-29 family targets both APP and BACE1, and its downregulation in AD cortex and hippocampus removes this brake, promoting amyloid formation.

    “The miR-29 family (miR-29a/b-1/c) targets both proteins, and its downregulation in AD cortex and hippocampus removes this brake, promoting amyloid formation (Fan et al., 2020; Hébert et al., 2008).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Fan et al., 2020

  • MiR-146a is elevated in reactive astrocytes in AD and is generally considered a compensatory anti-inflammatory regulator.

    “MiR-146a is also elevated in reactive astrocytes in AD and is generally considered a compensatory anti-inflammatory regulator.”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Fan et al., 2020

  • Neuron-derived EVs enriched in miR-132-3p or miR-124-3p can reprogram glial states, while glial EV cargo such as miR-155, miR-21-5p, and miR-146a feeds back onto neurons and other glia to propagate inflammatory or compensatory signals.

    “For example, neuron-derived EVs enriched in miR-132-3p or miR-124-3p can reprogram glial states, while glial EV cargo such as miR-155, miR-21-5p, and miR-146a feeds back onto neurons and other glia to propagate inflammatory or compensatory signals (Aloi et al., 2023; Cardoso et al., 2011; Fan et al., 2020; Gaudet et al., 2017; Guedes et al., 2014; Han et al., 2020; Lukiw et al., 2008; Saba et al.,”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Fan et al., 2020

  • In AD, the increase in miR-146a reflects an overwhelmed compensatory response rather than effective control, as chronic cytokine exposure renders the feedback loop insufficient to restore homeostasis.

    “In AD, however, this increase reflects an overwhelmed compensatory response rather than effective control, as chronic cytokine exposure renders the feedback loop insufficient to restore homeostasis (Fan et al., 2020).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Fan et al., 2020

  • MiR-146a serves as a classical NF-κB-induced negative-feedback regulator; elevated miR-146a in microglia acts to inhibit IRAK1 and TRAF6.

    “MiR-146a serves as a classical NF-κB–induced negative-feedback regulator. Elevated miR-146a in microglia acts to inhibit IRAK1 and TRAF6 (Fan et al., 2020; Lukiw et al., 2008; Saba et al., 2012; Saba et al., 2014).”

    From Cell-specific MicroRNA networks orchestrate the pathogenesis of Alzheimer’s disease (2026) · cites this paper as Fan et al., 2020

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Cited by

Sorted by citations

Authors
Fan, W., Liang, C., Ou, M., Zou, T., Sun, F., Zhou, H., & Cui, L.
Venue
Frontiers in Molecular Neuroscience
Publisher
Frontiers Media SA
Published
2020-06-05
Volume
13
ISSN
1662-5099
DOI
10.3389/fnmol.2020.00090
PMC
PMC7291868
Cited by
109
References
9
Licence
creativecommons.org/licenses/by/4.0/ (vor)

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