Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease

Research output: Contribution to journalReview articlepeer-review

Abstract / Description of output

Individuals diagnosed with Parkinson's disease (PD) often exhibit heightened susceptibility to cardiac dysfunction, reflecting a complex interaction between these conditions. The involvement of mitochondrial dysfunction in the development and progression of cardiac dysfunction and PD suggests a plausible commonality in some aspects of their molecular pathogenesis, potentially contributing to the prevalence of cardiac issues in PD. Mitochondria, crucial organelles responsible for energy production and cellular regulation, play important roles in tissues with high energetic demands, such as neurons and cardiac cells. Mitochondrial dysfunction can occur in different and non-mutually exclusive ways; however, some mechanisms include alterations in mitochondrial dynamics, compromised bioenergetics, biogenesis deficits, oxidative stress, impaired mitophagy, and disrupted calcium balance. It is plausible that these factors contribute to the increased prevalence of cardiac dysfunction in PD, suggesting mitochondrial health as a potential target for therapeutic intervention. This review provides an overview of the physiological mechanisms underlying mitochondrial quality control systems. It summarises the diverse roles of mitochondria in brain and heart function, highlighting shared pathways potentially exhibiting dysfunction and driving cardiac comorbidities in PD. By highlighting strategies to mitigate dysfunction associated with mitochondrial impairment in cardiac and neural tissues, our review aims to provide new perspectives on therapeutic approaches.

Original languageEnglish
Article number10973
Pages (from-to)1-30
Number of pages30
JournalInternational Journal of Molecular Sciences
Volume25
Issue number20
Early online date12 Oct 2024
DOIs
Publication statusPublished - Oct 2024

Keywords / Materials (for Non-textual outputs)

  • Humans
  • Parkinson Disease/metabolism
  • Oxidative Stress
  • Mitochondria/metabolism
  • Animals
  • Mitophagy
  • Heart Diseases/metabolism
  • Comorbidity
  • Energy Metabolism
  • Mitochondrial Dynamics
  • Mitochondria, Heart/metabolism

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