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Endothelial SRSF1 Promotes Ischemia-Induced Angiogenesis via ATF3-KLF2-S1PR1 Pathway.

Wenting Zhu1,2,3, Ning Xie1, Zhenyan Li1

  • 1Laboratory of Cardiovascular Science, Beijing Clinical Research Institute (W.Z., N.X., Z. Li, X.W., K.Z., R.D., L.G., Y.W., Y. Li, J.G., L.H., J.L., Y.J., W.A., Y. Liu, Z. Lin, C.-M.C.), Beijing Friendship Hospital, Capital Medical University, China.

Circulation Research
|November 6, 2025
PubMed
Summary

Serine/arginine splicing factor 1 (SRSF1) promotes angiogenesis in peripheral artery disease by regulating the ATF3-KLF2-S1PR1 pathway. Modulating SRSF1 offers a potential therapeutic strategy for ischemic vascular diseases.

Keywords:
angiogenesisendothelial cellshindlimbhypoxiaischemia

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Area of Science:

  • Vascular Biology
  • Molecular Mechanisms of Angiogenesis
  • RNA Splicing

Background:

  • Peripheral artery disease (PAD) is a severe ischemic condition lacking effective pharmacological treatments.
  • Improving angiogenesis to restore blood perfusion is a key therapeutic strategy for PAD.
  • Molecular mechanisms governing ischemia-induced angiogenesis in endothelial cells remain largely unknown.

Purpose of the Study:

  • To identify novel molecular regulators of ischemia-induced angiogenesis.
  • To investigate the role of serine/arginine splicing factor 1 (SRSF1) in endothelial cell function and angiogenesis.
  • To elucidate the downstream signaling pathways modulated by SRSF1 in response to ischemia.

Main Methods:

  • Discovery-driven proteomic analysis to identify ischemia-responsive proteins in endothelial cells.
  • In vivo hindlimb ischemia mouse model to assess angiogenesis and blood flow recovery.
  • In vitro assays (tube formation, migration, sprouting) using human endothelial cells.
  • Transcriptome sequencing, eCLIP-seq, RNA pull-down, and ChIP-qPCR to determine molecular mechanisms.

Main Results:

  • SRSF1 expression was elevated in endothelial cells following ischemia and responded to hypoxia.
  • Endothelial SRSF1 deficiency impaired angiogenesis and blood flow recovery in a mouse model.
  • SRSF1 overexpression enhanced endothelial angiogenic functions (tube formation, migration, sprouting) in vitro and in vivo.
  • SRSF1 directly bound ATF3 pre-mRNA, promoting full-length ATF3 and suppressing KLF2-S1PR1 signaling, thereby enhancing angiogenesis.
  • Alprostadil activated SRSF1 signaling, improving endothelial angiogenesis.

Conclusions:

  • SRSF1 is a novel regulator of ischemia-induced angiogenesis.
  • SRSF1 enhances endothelial angiogenic functions via the ATF3-KLF2-S1PR1 pathway.
  • Targeting endothelial SRSF1 presents a promising therapeutic avenue for ischemic vascular diseases.