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Peroxisome proliferator‑activated receptor γ coactivator‑1α in heart disease (Review)

Siyu Sun1, Huige Guo2, Guohui Chen1

  • 1Department of Cardiology, Life Science Center, The First Affiliated Hospital of Xinxiang Medical University, Weihui, Henan 453100, P.R. China.

Molecular Medicine Reports
|November 8, 2024
PubMed

Insights

Mitochondrial dysfunction contributes to heart disease (HD). Peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) regulates mitochondrial function, offering potential therapeutic targets for HD, though challenges remain.

Area of Science:

  • Cardiovascular Biology
  • Mitochondrial Medicine
  • Molecular Cardiology

Background:

  • Heart disease (HD) pathogenesis is linked to mitochondrial dysfunction.
  • Peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) is crucial for mitochondrial health.
  • PGC‑1α regulates mitochondrial biogenesis, energy metabolism, and oxidative stress.

Purpose of the Study:

  • To review the role of PGC‑1α in heart disease.
  • To explore signaling pathways controlling PGC‑1α activity in the heart.
  • To discuss PGC‑1α's therapeutic potential and challenges in treating various heart conditions.

Main Methods:

  • Literature review of studies on PGC‑1α and heart disease.
  • Analysis of signaling pathways (AMPK, SIRT1/3, NFκB) affecting PGC‑1α.
  • Examination of PGC‑1α's role in different types of heart disease.

Main Results:

  • PGC‑1α expression and activity are modulated by multiple signaling pathways.
  • PGC‑1α plays a significant role in heart failure, coronary heart disease, diabetic cardiomyopathy, cardiotoxicity, and arrhythmia.
  • Understanding PGC‑1α mechanisms can inform new therapeutic strategies for HD.

Conclusions:

  • PGC‑1α is a key regulator of cardiac mitochondrial function and is implicated in diverse heart diseases.
  • Targeting PGC‑1α presents therapeutic opportunities but also complexities requiring further investigation.
  • Further research into PGC‑1α's intricate mechanisms is essential for effective HD prevention and treatment.

Keywords:
energy metabolismheart diseasemitochondrialoxidative stressperoxisome proliferator‑activated receptor γ coactivator‑1α

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