FUNDC1: An Emerging Mitochondrial and MAMs Protein for Mitochondrial Quality Control in Heart Diseases

Xizhe Bai1,2, Zhe Zhang1,2, Xi Li1,2

  • 1Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai 200241, China.

Insights

Mitochondrial dysfunction contributes to heart disease (HD). This review highlights FUNDC1

Area of Science:

  • Mitochondrial biology
  • Cardiovascular research
  • Cellular quality control mechanisms

Background:

  • Heart diseases (HDs) are a leading global cause of death, often linked to mitochondrial dysfunction.
  • Mitochondrial Quality Control (MQC) is crucial for cellular health, with the FUNDC1 protein playing a key role.
  • FUNDC1's phosphorylation and expression levels impact cardiac injury, influencing various heart conditions.

Purpose of the Study:

  • To consolidate and summarize current evidence on the role of FUNDC1 in MQC.
  • To elucidate the association between FUNDC1 and prevalent heart diseases.
  • To explore the potential of exercise in modulating FUNDC1 activity for cardiovascular health.

Main Methods:

  • Literature review of studies investigating FUNDC1 in MQC and heart disease.
  • Analysis of research on FUNDC1 expression and phosphorylation in various cardiac conditions.
  • Examination of the link between exercise, the AMPK/FUNDC1 pathway, and cardiac function.

Main Results:

  • FUNDC1 expression is elevated in metabolic cardiomyopathy (MCM) but reduced in cardiac remodeling, heart failure, and ischemia-reperfusion (IR) injury.
  • FUNDC1 exhibits divergent effects on mitochondrial function across different heart diseases.
  • Exercise may enhance cardiac function via the AMPK/FUNDC1 pathway.

Conclusions:

  • FUNDC1 is a critical regulator in MQC with significant implications for heart disease pathogenesis.
  • Understanding FUNDC1's role offers insights into therapeutic strategies for various cardiac conditions.
  • Exercise emerges as a promising intervention, potentially mediated by the AMPK/FUNDC1 axis, for preventing and treating heart disease.

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