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  11. Interplay Between The Safe And The Sphingolipid Pathway For Cardioprotection

Interplay between the SAFE and the sphingolipid pathway for cardioprotection

Martin Cour1, Sarah Pedretti1, Frederic Nduhirabandi1

  • 1Hatter Institute/Cape Heart Institute, Department of Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.

Life Sciences
|October 14, 2024

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View abstract on PubMed

Summary
This summary is machine-generated.

Sphingosine kinase-1 (SK1) activation is crucial for the cardioprotective Survivor Activating Factor Enhancement (SAFE) pathway. Targeting SK1 may offer new strategies to improve heart survival after ischemia-reperfusion injury (IRI).

Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Cell Signaling

Background:

  • Cardioprotection against ischemia-reperfusion injury (IRI) involves the Survivor Activating Factor Enhancement (SAFE) pathway, including Tumor Necrosis Factor-alpha (TNF-α) and Signal Transducer and Activator of Transcription-3 (STAT-3).
  • The sphingolipid signaling pathway, involving sphingosine kinase-1 (SK1) and sphingosine-1 phosphate (S1P), also plays a key role in cardioprotection.

Purpose of the Study:

  • To investigate if the cardioprotective effect of exogenous S1P on the SAFE pathway is dependent on SK1 activation.
  • To elucidate the role of SK1 in mediating S1P-induced cardioprotection.

Main Methods:

  • Isolated cardiomyocytes and hearts from wild-type (WT), TNF-α knockout (KO), and STAT-3 KO mice were subjected to simulated ischemia or IRI.
  • Cells and hearts were treated with S1P and/or an SK1 inhibitor (SK1-I).
Keywords:
Ischemia-reperfusion injuryMitochondriaSignal transducer and activator of transcription 3Sphingolipid

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  • Cell viability, infarct size, and SK1 activity were assessed.

    • Main Results:

    • S1P pretreatment reduced cell death in WT mice, but this effect was abolished by SK1-I.
    • S1P failed to protect cardiomyocytes or hearts from TNF-α KO and STAT-3 KO mice against simulated ischemia/IRI.
    • S1P increased SK1 activity in WT and STAT-3 KO mice, but not in TNF-α KO mice.

    Conclusions:

    • Sphingosine kinase-1 (SK1) is essential for activating STAT-3 downstream of TNF-α within the SAFE pathway.
    • Targeting SK1 presents a potential therapeutic strategy for developing novel cardioprotective treatments against IRI.
    • These findings highlight the interplay between sphingolipid metabolism and the SAFE pathway in cardiac protection.
    Survivor activating factor enhancement pathway
    Tumor necrosis factor alpha