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Updated: Jun 24, 2025

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MiRNA let-7d-5p Alleviates Inflammatory Responses by Targeting Map3k1 and Inactivating ERK/p38 MAPK Signaling in

Fan Fang1, Cheng Chen2

  • 1Department of Geriatrics, Huangshi Central Hospital, Huangshi 435000, China.

Critical Reviews in Immunology
|June 7, 2024
PubMed

Insights

MicroRNA let-7d-5p is downregulated in Alzheimer's disease (AD). Upregulating this microRNA may help treat AD by reducing neuroinflammation via the Map3k1/ERK/p38 MAPK pathway.

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alzheimer's disease (AD) is a leading cause of dementia.
  • MicroRNAs (miRNAs) are implicated in AD pathogenesis.
  • let-7d-5p was found to be downregulated in AD patients.

Purpose of the Study:

  • Investigate the function and mechanisms of let-7d-5p in AD.
  • Determine the role of let-7d-5p in microglial activation and neuroinflammation.
  • Explore let-7d-5p as a potential therapeutic target for AD.

Main Methods:

  • Used amyloid-beta (Aβ)1-42-treated BV2 cells as an in vitro AD model.
  • Assessed let-7d-5p levels and microglial phenotype.
  • Verified let-7d-5p binding to Map3k1 using luciferase reporter assays.
  • Analyzed the effect of let-7d-5p on ERK/p38 MAPK signaling.

Main Results:

  • let-7d-5p was downregulated in Aβ1-42-stimulated microglial cells.
  • Upregulation of let-7d-5p promoted microglial M1 to M2 phenotype transition.
  • let-7d-5p directly targets Map3k1 3'UTR.
  • let-7d-5p inactivates ERK/p38 MAPK signaling.

Conclusions:

  • let-7d-5p plays a crucial role in regulating microglial neuroinflammation in AD.
  • let-7d-5p may serve as a novel diagnostic and therapeutic target for AD.
  • The let-7d-5p/Map3k1 axis modulates microglial activation and neuroinflammation in AD.

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