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RNA Splicing01:32

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Splicing is the process by which eukaryotic RNA is edited before its translation into protein. The RNA strand transcribed from eukaryotic DNA is called the primary transcript. The primary transcripts that become mRNAs are called precursor messenger RNAs (pre-mRNAs). Eukaryotic pre-mRNA contains alternating sequences of exons and introns. Exons are nucleotide sequences that code for proteins, whereas introns are the non-coding regions. In RNA splicing, introns are removed and exons are bonded...
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Alternative RNA splicing is the regulated splicing of exons and introns to produce different mature mRNAs from a single pre-mRNA. Unlike in constitutive splicing where a single gene produces a single type of mRNA, alternative splicing allows an organism to produce multiple proteins from a single gene and plays an important role in protein diversity.
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In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
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Inflammatory signaling attenuates spliceosome function and cognitive ability.

Lan Lin1, Xiaoya Huang2, Chunhua Huang1

  • 1Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Renmin Hospital of Wuhan University, Wuhan, Hubei, China.

Autophagy
|September 18, 2025
PubMed
Summary
This summary is machine-generated.

Inflammation triggers cognitive impairment by activating FGF2 signaling, which impairs autophagy and leads to toxic oligomer buildup in the brain. Restoring autophagy rescues cognitive function.

Keywords:
Autophagybraincognitive impairmentinflammationnucleusspliceosome

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Immunology

Background:

  • Cognitive impairment mechanisms are complex and not fully understood.
  • Inflammation is implicated in cognitive decline, but the precise pathways are unclear.

Purpose of the Study:

  • To investigate the role of inflammation-induced FGF2 signaling in cognitive impairment.
  • To elucidate the molecular mechanisms linking inflammation, FGF2, autophagy, and cognitive dysfunction.

Main Methods:

  • Utilized mouse models of coronavirus disease 2019 (COVID-19) and acute kidney injury (AKI)-induced inflammation.
  • Analyzed APP cleavage product oligomers, FGF2 activation, HNRNPA1 localization, and autophagy markers (ATG16L1).
  • Investigated the effects of FGF2 inhibition (erdafitinib) and FGF2 knockout on cognitive function and autophagy.

Main Results:

  • Inflammation induced brain oligomer accumulation and cognitive impairment, linked to FGF2 activation.
  • FGF2 activation caused HNRNPA1 cytoplasmic translocation and degradation, impairing autophagy and ATG16L1 splicing.
  • FGF2 inhibition or knockout restored autophagy and rescued cognitive impairment in inflammation models.

Conclusions:

  • Inflammation activates FGF2 signaling, which suppresses autophagy via HNRNPA1 and aberrant ATG16L1 splicing.
  • This pathway leads to oligomer accumulation and cognitive impairment.
  • Targeting FGF2 signaling represents a potential therapeutic strategy for inflammation-associated cognitive dysfunction.