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Pandora's Box: mitochondrial defects in ischaemic heart disease and stroke
Sasan Andalib1, Afshin A Divani2, Tanja M Michel3
1Neuroscience Research Center, Department of Neurosurgery, Poursina Hospital,School of Medicine,Guilan University of Medical Sciences,Rasht,Iran.
Insights
Mitochondria and mitochondrial DNA (mtDNA) play a significant role in ischaemic heart disease and stroke. Research is exploring these molecular links and mtDNA alterations in vascular event development.
Area of Science:
- Cardiovascular Science
- Mitochondrial Biology
- Genetics
Background:
- Ischaemic heart disease and stroke are leading global vascular events with complex pathogenesis.
- Mitochondrial involvement, including reactive oxygen species and pericyte impact, is increasingly recognized.
- While nuclear gene roles are established, mitochondrial DNA's (mtDNA) contribution to these disorders is less understood.
Purpose of the Study:
- To explore the molecular events and mitochondrial DNA (mtDNA) alterations in ischaemic heart disease and stroke.
- To elucidate the role of mitochondria in the pathophysiology of these vascular events.
- To highlight the growing evidence for mitochondria and mtDNA involvement in vascular disease.
Main Methods:
- Review of recent genetic and epigenetic findings.
- Analysis of molecular mechanisms involving mitochondria.
- Exploration of mitochondrial DNA (mtDNA) alterations.
Main Results:
- Mitochondrial reactive oxygen species contribute to pathogenesis via oxidized LDL and apoptosis.
- Mitochondria impact pericytes, directly influencing ischaemic heart disease and stroke development.
- Emerging evidence links mitochondria and mtDNA alterations to vascular events, suggesting a larger role than previously thought.
Conclusions:
- Mitochondria and their DNA (mtDNA) are critically involved in the pathogenesis of ischaemic heart disease and stroke.
- Further research into mtDNA alterations and mitochondrial function is crucial for understanding and potentially treating these vascular events.
- The complex interplay between nuclear and mitochondrial factors warrants continued investigation.
Abstract:
Ischaemic heart disease and stroke are vascular events with serious health consequences worldwide. Recent genetic and epigenetic techniques have revealed many genetic determinants of these vascular events and simplified the approaches to research focused on ischaemic heart disease and stroke. The pathogenetic mechanisms of ischaemic heart disease and stroke are complex, with mitochondrial involvement (partially or entirely) recently gaining substantial support. Not only can mitochondrial reactive oxygen species give rise to ischaemic heart disease and stroke by production of oxidised low-density lipoprotein and induction of apoptosis, but the impact on pericytes contributes directly to the pathogenesis. Over the past two decades, publications implicate the causative role of nuclear genes in the development of ischaemic heart disease and stroke, in contrast to the potential role of mitochondrial DNA (mtDNA) in the pathophysiology of the disorders, which is much less understood, although recent studies do demonstrate that the involvement of mitochondria and mtDNA in the development of ischaemic heart disease and stroke is likely to be larger than originally thought, with the novel discovery of links among mitochondria, mtDNA and vascular events. Here we explore the molecular events and mtDNA alterations in relation to the role of mitochondria in ischaemic heart disease and stroke.