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Related Experiment Video

Updated: Jun 27, 2025

Author Spotlight: Unveiling Oxidative Phosphorylation System Dynamics and Mitochondrial Roles in Health and Disease
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SPTLC3 Is Essential for Complex I Activity and Contributes to Ischemic Cardiomyopathy.

Anna Kovilakath1, Adolfo G Mauro2, Yolander A Valentine3,4

  • 1Department of Human and Molecular Genetics (A.K., M.J., J.J.W., M.A.S.), Virginia Commonwealth University, Richmond.

Circulation
|April 25, 2024
PubMed
Summary
This summary is machine-generated.

Serine palmitoyltransferase subunit 3 (SPTLC3) is induced in ischemic cardiomyopathy, producing atypical sphingolipids that impair cardiac function. Depleting SPTLC3 improves cardiac function and survival by enhancing mitochondrial complex I activity.

Keywords:
cardiomyopathyelectron transport complex Imitochondriaserine C-palmitoyltransferasesphingolipids

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Area of Science:

  • Cardiovascular Biology
  • Metabolic Disease
  • Mitochondrial Function

Background:

  • Dysregulated sphingolipid metabolism is linked to cardiovascular disease, but specific roles remain unclear.
  • Sphingolipids are synthesized by serine palmitoyltransferase (SPT) enzymes, including canonical SPTLC1/2 and noncanonical SPTLC3.
  • SPTLC3 produces atypical (d16) sphingolipids, distinct from canonical (d18) sphingolipids.

Purpose of the Study:

  • To investigate the role of SPTLC3 in ischemic cardiomyopathy.
  • To determine the impact of SPTLC3-derived sphingolipids on cardiac function and mitochondrial activity.
  • To elucidate the regulatory mechanisms of SPTLC3 induction under ischemic conditions.

Main Methods:

  • Targeted lipidomics in human and mouse models of ischemic cardiomyopathy.
  • Chromatin immunoprecipitation to assess HIF1α regulation of SPTLC3.
  • Generation and analysis of cardiomyocyte-specific SPTLC3 knockout (cSPTLC3KO) mice.
  • Assessment of cardiac function, metabolism, mitochondrial properties, and myocardial infarction in cSPTLC3KO mice.

Main Results:

  • SPTLC3 is upregulated in ischemic cardiomyopathy, leading to atypical sphingolipid production and altered cellular sphingolipid composition.
  • HIF1α transcriptionally regulates SPTLC3 under ischemic conditions.
  • Cardiomyocyte-specific SPTLC3 depletion attenuates cardiac fibrosis, hypertrophy, and oxidative stress, improving cardiac function and survival.
  • SPTLC3 depletion alters mitochondrial complex I composition and activity, impacting the electron transport chain.

Conclusions:

  • SPTLC3 plays a critical role in regulating mitochondrial complex I activity and electron transport chain function.
  • SPTLC3 contributes to ischemic injury by modulating mitochondrial function.
  • Targeting SPTLC3 may offer a novel therapeutic strategy for cardiovascular disease.