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Cardiolipin Remodeling in Cardiovascular Diseases: Implication for Mitochondrial Dysfunction.

Huijie Zhang1, Fengzhi Yu1, Zhenjun Tian2

  • 1School of Exercise and Health, Shanghai University of Sport, Shanghai, China.

Acta Physiologica (Oxford, England)
|June 18, 2025
PubMed
Summary

Cardiolipin remodeling is key to mitochondrial health in cardiovascular diseases (CVDs). Disruptions in this process drive dysfunction, but targeting cardiolipin offers promising therapeutic strategies for CVDs.

Keywords:
ALCAT1cardiolipin remodelingcardiovascular diseasesmitochondrial dysfunctiontafazzin

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Area of Science:

  • Mitochondrial Biology
  • Cardiovascular Research
  • Biochemistry

Background:

  • Mitochondrial dysfunction is central to cardiovascular diseases (CVDs).
  • Cardiolipin (CL), a vital mitochondrial phospholipid, regulates key functions like energy production and membrane integrity.
  • CL requires remodeling for proper acyl composition, and its disruption impairs mitochondrial function.

Purpose of the Study:

  • To review the role of cardiolipin remodeling in mitochondrial dysfunction within CVDs.
  • To explore the impact of CL remodeling enzyme deficiencies on CVD pathogenesis.

Main Methods:

  • Review of literature on CL function and its role in CVDs.
  • Examination of CL remodeling enzymes: tafazzin (TAZ), ALCAT1, and MLCLAT1.
  • Analysis of CL homeostasis, mitochondrial function, and CVD pathogenesis.

Main Results:

  • Correct CL function is essential for mitochondrial health and cardioprotection.
  • Defects in TAZ, ALCAT1, or MLCLAT1 lead to pathological CL remodeling, driving mitochondrial dysfunction and CVD progression.
  • CL-based therapeutic strategies, including gene therapy and pharmacotherapy, are emerging.

Conclusions:

  • Targeting cardiolipin represents a potential therapeutic avenue for cardiovascular diseases.
  • Understanding CL remodeling is crucial for developing novel CVD treatments.