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Ythdc1-p300-Klf5 Complex-Mediated Golgi Dysfunction Promotes Aortic Aneurysm.

Wen-Li Wang1,2, Zhi-Xue Song1, Si-Ming Bu1

  • 1Department of Biochemistry and Molecular Biology, Key Laboratory of Neural and Vascular Biology, Ministry of Education, and Hebei Key Laboratory of Cardiovascular Homeostasis and Aging, Hebei Medical University, Shijiazhuang, Hebei, 050017, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|November 29, 2025
PubMed
Summary
This summary is machine-generated.

Klf5 upregulates Golph3l, promoting Golgi compaction and apoptosis-induced proliferation in vascular smooth muscle cells, driving aortic aneurysm development. Targeting this pathway offers a potential therapeutic strategy for aortic diseases.

Keywords:
AAADGolph3lKLF5m6A VSMC

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Area of Science:

  • Vascular Biology
  • Molecular Biology
  • Genetics

Background:

  • Klf5 and Golph3l regulate Golgi morphology, impacting vascular smooth muscle cell (VSMC) apoptosis and contributing to aortic aneurysm.
  • The precise molecular mechanisms linking Klf5, Golph3l, and Golgi alterations in aneurysms remain elusive.

Purpose of the Study:

  • To elucidate the molecular link between Klf5, Golph3l, and Golgi morphology in the context of aortic aneurysm.
  • To investigate the role of apoptosis-induced proliferation (AIP) in VSMCs during aortic dissection (AD) and aneurysm.
  • To identify therapeutic targets for aortic aneurysm.

Main Methods:

  • Investigated Klf5 and Golph3l roles in VSMC apoptosis and Golgi morphology.
  • Analyzed Angiotensin II (AngII) stimulation effects on VSMCs.
  • Examined m6A RNA modification, specifically m6A-Gm40097, and its interaction with Klf5, Ythdc1, and p300.
  • Developed a predictive website for AD patient outcomes.

Main Results:

  • Apoptosis-induced proliferation (AIP) in VSMCs is observed in human and mouse AD and aneurysms.
  • Klf5-induced Golph3l upregulation drives Golgi compaction, facilitating TNF-α and TNFSF12 secretion, essential for AIP and aneurysm.
  • AngII-induced m6A RNA elevation, particularly m6A-Gm40097, upregulates Golph3l and promotes AIP.
  • m6A-Gm40097 facilitates Klf5-Ythdc1-p300 complex formation on the Golph3l promoter, activating transcription.
  • A predictive website for post-operative AD mortality was established.

Conclusions:

  • A novel regulatory mechanism involving lncRNA m6A modification, chromatin remodeling, and transcription activation is identified.
  • Targeting the Ythdc1-p300-Klf5 complex presents a potential therapeutic strategy for Golgi dysfunction and aortic aneurysm.
  • The findings provide insights into AD pathogenesis and risk stratification.